https://centre.santafe.edu/complextime/w/index.php?title=Cognitive_Regime_Shift_II_-_When/why/how_the_Brain_Breaks&feed=atom&action=historyCognitive Regime Shift II - When/why/how the Brain Breaks - Revision history2024-03-29T10:44:13ZRevision history for this page on the wikiMediaWiki 1.35.6https://centre.santafe.edu/complextime/w/index.php?title=Cognitive_Regime_Shift_II_-_When/why/how_the_Brain_Breaks&diff=5531&oldid=prevAmyPChen at 20:47, May 21, 20202020-05-21T20:47:21Z<p></p>
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<tr><td class='diff-marker'>−</td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>|Meeting video=https://<del class="diffchange diffchange-inline">youtu</del>.<del class="diffchange diffchange-inline">be</del>/TwL5IMkNrwk</div></td><td class='diff-marker'>+</td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>|Meeting video=https://<ins class="diffchange diffchange-inline">www</ins>.<ins class="diffchange diffchange-inline">youtube.com</ins>/<ins class="diffchange diffchange-inline">watch?v=</ins>TwL5IMkNrwk<ins class="diffchange diffchange-inline">&list=PLZlVBTf7N6GoAPu-80tFHGLD39e3uidj3&index=13</ins></div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Organizers=StevenPetersen;DavidKrakauer;JohnKrakauer</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Organizers=StevenPetersen;DavidKrakauer;JohnKrakauer</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Meeting summary=In this second working group on the brain we shall build on some of the foundational discussions raised in the first meeting. These included significant debate around the merits of correlation vs. causation, indicators or indices of the loss of function, and the relationship among levels required to explain failure - from the genetic and cellular to the cognitive and behavioral (including states such as sleep and anesthesia). Mechanisms of loss of function discussed will range from cell to network drop-out. We shall return to some of the key questions that motivated the first meeting with a better sense of the limitations of data sets and tools of analysis. This includes the synthesis and integration of neurology with several areas of complexity science to include adaptation and robustness in system aging, early network-based indicators for risk factors, the application of criticality and related tipping point to regime shifts, the measurement of long-range order and disorder across the brain, and methods for analyzing collective dynamics in the aging and diseased brain. </div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Meeting summary=In this second working group on the brain we shall build on some of the foundational discussions raised in the first meeting. These included significant debate around the merits of correlation vs. causation, indicators or indices of the loss of function, and the relationship among levels required to explain failure - from the genetic and cellular to the cognitive and behavioral (including states such as sleep and anesthesia). Mechanisms of loss of function discussed will range from cell to network drop-out. We shall return to some of the key questions that motivated the first meeting with a better sense of the limitations of data sets and tools of analysis. This includes the synthesis and integration of neurology with several areas of complexity science to include adaptation and robustness in system aging, early network-based indicators for risk factors, the application of criticality and related tipping point to regime shifts, the measurement of long-range order and disorder across the brain, and methods for analyzing collective dynamics in the aging and diseased brain. </div></td></tr>
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</table>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Cognitive_Regime_Shift_II_-_When/why/how_the_Brain_Breaks&diff=5530&oldid=prevAmyPChen at 20:43, May 21, 20202020-05-21T20:43:58Z<p></p>
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<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Organizers=StevenPetersen;DavidKrakauer;JohnKrakauer</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Organizers=StevenPetersen;DavidKrakauer;JohnKrakauer</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Meeting summary=In this second working group on the brain we shall build on some of the foundational discussions raised in the first meeting. These included significant debate around the merits of correlation vs. causation, indicators or indices of the loss of function, and the relationship among levels required to explain failure - from the genetic and cellular to the cognitive and behavioral (including states such as sleep and anesthesia). Mechanisms of loss of function discussed will range from cell to network drop-out. We shall return to some of the key questions that motivated the first meeting with a better sense of the limitations of data sets and tools of analysis. This includes the synthesis and integration of neurology with several areas of complexity science to include adaptation and robustness in system aging, early network-based indicators for risk factors, the application of criticality and related tipping point to regime shifts, the measurement of long-range order and disorder across the brain, and methods for analyzing collective dynamics in the aging and diseased brain. </div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Meeting summary=In this second working group on the brain we shall build on some of the foundational discussions raised in the first meeting. These included significant debate around the merits of correlation vs. causation, indicators or indices of the loss of function, and the relationship among levels required to explain failure - from the genetic and cellular to the cognitive and behavioral (including states such as sleep and anesthesia). Mechanisms of loss of function discussed will range from cell to network drop-out. We shall return to some of the key questions that motivated the first meeting with a better sense of the limitations of data sets and tools of analysis. This includes the synthesis and integration of neurology with several areas of complexity science to include adaptation and robustness in system aging, early network-based indicators for risk factors, the application of criticality and related tipping point to regime shifts, the measurement of long-range order and disorder across the brain, and methods for analyzing collective dynamics in the aging and diseased brain. </div></td></tr>
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</table>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Cognitive_Regime_Shift_II_-_When/why/how_the_Brain_Breaks&diff=5523&oldid=prevAmyPChen at 22:11, May 14, 20202020-05-14T22:11:08Z<p></p>
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<tr><td colspan="2"> </td><td class='diff-marker'>+</td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">|Meeting video=https://www.youtube.com/watch?v=HnA91mymghA&feature=youtu.be</ins></div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Organizers=StevenPetersen;DavidKrakauer;JohnKrakauer</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Organizers=StevenPetersen;DavidKrakauer;JohnKrakauer</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Meeting summary=In this second working group on the brain we shall build on some of the foundational discussions raised in the first meeting. These included significant debate around the merits of correlation vs. causation, indicators or indices of the loss of function, and the relationship among levels required to explain failure - from the genetic and cellular to the cognitive and behavioral (including states such as sleep and anesthesia). Mechanisms of loss of function discussed will range from cell to network drop-out. We shall return to some of the key questions that motivated the first meeting with a better sense of the limitations of data sets and tools of analysis. This includes the synthesis and integration of neurology with several areas of complexity science to include adaptation and robustness in system aging, early network-based indicators for risk factors, the application of criticality and related tipping point to regime shifts, the measurement of long-range order and disorder across the brain, and methods for analyzing collective dynamics in the aging and diseased brain. </div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Meeting summary=In this second working group on the brain we shall build on some of the foundational discussions raised in the first meeting. These included significant debate around the merits of correlation vs. causation, indicators or indices of the loss of function, and the relationship among levels required to explain failure - from the genetic and cellular to the cognitive and behavioral (including states such as sleep and anesthesia). Mechanisms of loss of function discussed will range from cell to network drop-out. We shall return to some of the key questions that motivated the first meeting with a better sense of the limitations of data sets and tools of analysis. This includes the synthesis and integration of neurology with several areas of complexity science to include adaptation and robustness in system aging, early network-based indicators for risk factors, the application of criticality and related tipping point to regime shifts, the measurement of long-range order and disorder across the brain, and methods for analyzing collective dynamics in the aging and diseased brain. </div></td></tr>
</table>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Cognitive_Regime_Shift_II_-_When/why/how_the_Brain_Breaks&diff=5106&oldid=prevAmyPChen at 00:37, November 14, 20192019-11-14T00:37:37Z<p></p>
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<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* Ehren Newman: Taking seriously the idea that complex systems exist in their own right leads to the idea that functional failure can result from degeneration at the systems-level without clear connection to individual constituent processes. How does a hypothesis that exists at this level survive in a scientific community driven first and foremost by reductionism and demands silver-bullet solutions to neurodegenerative disorders? Practically, what empirical data would prove the necessity of a systems-level perspective over a reductionistic one? To ask this question another way, given the multiple levels at which a problem can be studied (e.g., in neuroscience: organismal > systems > cellular > molecular > genetic) is there a general approach to empirically establish the level at which a phenomenon of interest (e.g., Alzheimer’s disease) is most clearly resolved? If functional failure were proven to result from systems-level degeneration without clear links to individual constituent processes, thus making individual molecular targets tangentially relevant, what treatment approaches hold the greatest promise? </div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* Ehren Newman: Taking seriously the idea that complex systems exist in their own right leads to the idea that functional failure can result from degeneration at the systems-level without clear connection to individual constituent processes. How does a hypothesis that exists at this level survive in a scientific community driven first and foremost by reductionism and demands silver-bullet solutions to neurodegenerative disorders? Practically, what empirical data would prove the necessity of a systems-level perspective over a reductionistic one? To ask this question another way, given the multiple levels at which a problem can be studied (e.g., in neuroscience: organismal > systems > cellular > molecular > genetic) is there a general approach to empirically establish the level at which a phenomenon of interest (e.g., Alzheimer’s disease) is most clearly resolved? If functional failure were proven to result from systems-level degeneration without clear links to individual constituent processes, thus making individual molecular targets tangentially relevant, what treatment approaches hold the greatest promise? </div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Location=Santa Fe Institute</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Location=Santa Fe Institute</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>|Attendee list=JacopoGrilli;CaterinaGratton;DietmarPlenz;SusanFitzpatrick;RobertoCabeza;JackGallant;RussPoldrack;PaulGarcia;RandyMcIntosh;ViktorJirsa;RichardFrackowiak;NikolausKriegeskorte;SidneyRedner;NihatAy;Ehren Newman;GuyMiller;Tyler Marghetis</div></td><td class='diff-marker'>+</td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>|Attendee list=JacopoGrilli;CaterinaGratton;DietmarPlenz;SusanFitzpatrick;RobertoCabeza;JackGallant;RussPoldrack;PaulGarcia;RandyMcIntosh;ViktorJirsa;RichardFrackowiak;NikolausKriegeskorte;SidneyRedner;NihatAy;Ehren Newman;GuyMiller;Tyler Marghetis<ins class="diffchange diffchange-inline">;ArtemyKolchinsky</ins></div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Post-meeting summary=Coming soon.</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Post-meeting summary=Coming soon.</div></td></tr>
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</table>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Cognitive_Regime_Shift_II_-_When/why/how_the_Brain_Breaks&diff=5104&oldid=prevAmyPChen at 00:35, November 14, 20192019-11-14T00:35:57Z<p></p>
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<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* Ehren Newman: Taking seriously the idea that complex systems exist in their own right leads to the idea that functional failure can result from degeneration at the systems-level without clear connection to individual constituent processes. How does a hypothesis that exists at this level survive in a scientific community driven first and foremost by reductionism and demands silver-bullet solutions to neurodegenerative disorders? Practically, what empirical data would prove the necessity of a systems-level perspective over a reductionistic one? To ask this question another way, given the multiple levels at which a problem can be studied (e.g., in neuroscience: organismal > systems > cellular > molecular > genetic) is there a general approach to empirically establish the level at which a phenomenon of interest (e.g., Alzheimer’s disease) is most clearly resolved? If functional failure were proven to result from systems-level degeneration without clear links to individual constituent processes, thus making individual molecular targets tangentially relevant, what treatment approaches hold the greatest promise? </div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* Ehren Newman: Taking seriously the idea that complex systems exist in their own right leads to the idea that functional failure can result from degeneration at the systems-level without clear connection to individual constituent processes. How does a hypothesis that exists at this level survive in a scientific community driven first and foremost by reductionism and demands silver-bullet solutions to neurodegenerative disorders? Practically, what empirical data would prove the necessity of a systems-level perspective over a reductionistic one? To ask this question another way, given the multiple levels at which a problem can be studied (e.g., in neuroscience: organismal > systems > cellular > molecular > genetic) is there a general approach to empirically establish the level at which a phenomenon of interest (e.g., Alzheimer’s disease) is most clearly resolved? If functional failure were proven to result from systems-level degeneration without clear links to individual constituent processes, thus making individual molecular targets tangentially relevant, what treatment approaches hold the greatest promise? </div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Location=Santa Fe Institute</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Location=Santa Fe Institute</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>|Attendee list=JacopoGrilli;CaterinaGratton;DietmarPlenz;SusanFitzpatrick;RobertoCabeza;JackGallant;RussPoldrack;PaulGarcia;RandyMcIntosh;ViktorJirsa;RichardFrackowiak;NikolausKriegeskorte;SidneyRedner;NihatAy;Ehren Newman;GuyMiller;Tyler Marghetis<del class="diffchange diffchange-inline">;AmyPChen2</del></div></td><td class='diff-marker'>+</td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>|Attendee list=JacopoGrilli;CaterinaGratton;DietmarPlenz;SusanFitzpatrick;RobertoCabeza;JackGallant;RussPoldrack;PaulGarcia;RandyMcIntosh;ViktorJirsa;RichardFrackowiak;NikolausKriegeskorte;SidneyRedner;NihatAy;Ehren Newman;GuyMiller;Tyler Marghetis</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Post-meeting summary=Coming soon.</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Post-meeting summary=Coming soon.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>}}</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>}}</div></td></tr>
</table>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Cognitive_Regime_Shift_II_-_When/why/how_the_Brain_Breaks&diff=5102&oldid=prevAmyPChen at 00:33, November 14, 20192019-11-14T00:33:41Z<p></p>
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 00:33, November 14, 2019</td>
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<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Attendee list=JacopoGrilli;CaterinaGratton;DietmarPlenz;SusanFitzpatrick;RobertoCabeza;JackGallant;RussPoldrack;PaulGarcia;RandyMcIntosh;ViktorJirsa;RichardFrackowiak;NikolausKriegeskorte;SidneyRedner;NihatAy;Ehren Newman;GuyMiller;Tyler Marghetis;AmyPChen2</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Attendee list=JacopoGrilli;CaterinaGratton;DietmarPlenz;SusanFitzpatrick;RobertoCabeza;JackGallant;RussPoldrack;PaulGarcia;RandyMcIntosh;ViktorJirsa;RichardFrackowiak;NikolausKriegeskorte;SidneyRedner;NihatAy;Ehren Newman;GuyMiller;Tyler Marghetis;AmyPChen2</div></td></tr>
<tr><td colspan="2"> </td><td class='diff-marker'>+</td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">|Post-meeting summary=Coming soon.</ins></div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>}}</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>}}</div></td></tr>
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</table>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Cognitive_Regime_Shift_II_-_When/why/how_the_Brain_Breaks&diff=5079&oldid=prevWikiworks at 14:04, November 12, 20192019-11-12T14:04:26Z<p></p>
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 14:04, November 12, 2019</td>
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<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* Ehren Newman: Taking seriously the idea that complex systems exist in their own right leads to the idea that functional failure can result from degeneration at the systems-level without clear connection to individual constituent processes. How does a hypothesis that exists at this level survive in a scientific community driven first and foremost by reductionism and demands silver-bullet solutions to neurodegenerative disorders? Practically, what empirical data would prove the necessity of a systems-level perspective over a reductionistic one? To ask this question another way, given the multiple levels at which a problem can be studied (e.g., in neuroscience: organismal > systems > cellular > molecular > genetic) is there a general approach to empirically establish the level at which a phenomenon of interest (e.g., Alzheimer’s disease) is most clearly resolved? If functional failure were proven to result from systems-level degeneration without clear links to individual constituent processes, thus making individual molecular targets tangentially relevant, what treatment approaches hold the greatest promise? </div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* Ehren Newman: Taking seriously the idea that complex systems exist in their own right leads to the idea that functional failure can result from degeneration at the systems-level without clear connection to individual constituent processes. How does a hypothesis that exists at this level survive in a scientific community driven first and foremost by reductionism and demands silver-bullet solutions to neurodegenerative disorders? Practically, what empirical data would prove the necessity of a systems-level perspective over a reductionistic one? To ask this question another way, given the multiple levels at which a problem can be studied (e.g., in neuroscience: organismal > systems > cellular > molecular > genetic) is there a general approach to empirically establish the level at which a phenomenon of interest (e.g., Alzheimer’s disease) is most clearly resolved? If functional failure were proven to result from systems-level degeneration without clear links to individual constituent processes, thus making individual molecular targets tangentially relevant, what treatment approaches hold the greatest promise? </div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Location=Santa Fe Institute</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Location=Santa Fe Institute</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>|Attendee list=JacopoGrilli;CaterinaGratton;DietmarPlenz;SusanFitzpatrick;RobertoCabeza;JackGallant;RussPoldrack;PaulGarcia;RandyMcIntosh;ViktorJirsa;RichardFrackowiak;NikolausKriegeskorte;SidneyRedner;NihatAy;Ehren Newman;<del class="diffchange diffchange-inline">Guy Miller</del>;Tyler Marghetis;AmyPChen2</div></td><td class='diff-marker'>+</td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>|Attendee list=JacopoGrilli;CaterinaGratton;DietmarPlenz;SusanFitzpatrick;RobertoCabeza;JackGallant;RussPoldrack;PaulGarcia;RandyMcIntosh;ViktorJirsa;RichardFrackowiak;NikolausKriegeskorte;SidneyRedner;NihatAy;Ehren Newman;<ins class="diffchange diffchange-inline">GuyMiller</ins>;Tyler Marghetis;AmyPChen2</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>}}</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>}}</div></td></tr>
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</table>Wikiworkshttps://centre.santafe.edu/complextime/w/index.php?title=Cognitive_Regime_Shift_II_-_When/why/how_the_Brain_Breaks&diff=5068&oldid=prevAmyPChen at 19:37, November 11, 20192019-11-11T19:37:55Z<p></p>
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 19:37, November 11, 2019</td>
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<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* Ehren Newman: Taking seriously the idea that complex systems exist in their own right leads to the idea that functional failure can result from degeneration at the systems-level without clear connection to individual constituent processes. How does a hypothesis that exists at this level survive in a scientific community driven first and foremost by reductionism and demands silver-bullet solutions to neurodegenerative disorders? Practically, what empirical data would prove the necessity of a systems-level perspective over a reductionistic one? To ask this question another way, given the multiple levels at which a problem can be studied (e.g., in neuroscience: organismal > systems > cellular > molecular > genetic) is there a general approach to empirically establish the level at which a phenomenon of interest (e.g., Alzheimer’s disease) is most clearly resolved? If functional failure were proven to result from systems-level degeneration without clear links to individual constituent processes, thus making individual molecular targets tangentially relevant, what treatment approaches hold the greatest promise? </div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* Ehren Newman: Taking seriously the idea that complex systems exist in their own right leads to the idea that functional failure can result from degeneration at the systems-level without clear connection to individual constituent processes. How does a hypothesis that exists at this level survive in a scientific community driven first and foremost by reductionism and demands silver-bullet solutions to neurodegenerative disorders? Practically, what empirical data would prove the necessity of a systems-level perspective over a reductionistic one? To ask this question another way, given the multiple levels at which a problem can be studied (e.g., in neuroscience: organismal > systems > cellular > molecular > genetic) is there a general approach to empirically establish the level at which a phenomenon of interest (e.g., Alzheimer’s disease) is most clearly resolved? If functional failure were proven to result from systems-level degeneration without clear links to individual constituent processes, thus making individual molecular targets tangentially relevant, what treatment approaches hold the greatest promise? </div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Location=Santa Fe Institute</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Location=Santa Fe Institute</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>|Attendee list=JacopoGrilli;CaterinaGratton;DietmarPlenz;SusanFitzpatrick;RobertoCabeza;JackGallant;RussPoldrack;PaulGarcia;RandyMcIntosh;ViktorJirsa;RichardFrackowiak;NikolausKriegeskorte;SidneyRedner;NihatAy;Ehren Newman;Guy Miller;Tyler Marghetis</div></td><td class='diff-marker'>+</td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>|Attendee list=JacopoGrilli;CaterinaGratton;DietmarPlenz;SusanFitzpatrick;RobertoCabeza;JackGallant;RussPoldrack;PaulGarcia;RandyMcIntosh;ViktorJirsa;RichardFrackowiak;NikolausKriegeskorte;SidneyRedner;NihatAy;Ehren Newman;Guy Miller;Tyler Marghetis<ins class="diffchange diffchange-inline">;AmyPChen2</ins></div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>}}</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>}}</div></td></tr>
</table>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Cognitive_Regime_Shift_II_-_When/why/how_the_Brain_Breaks&diff=5057&oldid=prevAmyPChen at 18:54, November 11, 20192019-11-11T18:54:51Z<p></p>
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 18:54, November 11, 2019</td>
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<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* Ehren Newman: Taking seriously the idea that complex systems exist in their own right leads to the idea that functional failure can result from degeneration at the systems-level without clear connection to individual constituent processes. How does a hypothesis that exists at this level survive in a scientific community driven first and foremost by reductionism and demands silver-bullet solutions to neurodegenerative disorders? Practically, what empirical data would prove the necessity of a systems-level perspective over a reductionistic one? To ask this question another way, given the multiple levels at which a problem can be studied (e.g., in neuroscience: organismal > systems > cellular > molecular > genetic) is there a general approach to empirically establish the level at which a phenomenon of interest (e.g., Alzheimer’s disease) is most clearly resolved? If functional failure were proven to result from systems-level degeneration without clear links to individual constituent processes, thus making individual molecular targets tangentially relevant, what treatment approaches hold the greatest promise? </div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* Ehren Newman: Taking seriously the idea that complex systems exist in their own right leads to the idea that functional failure can result from degeneration at the systems-level without clear connection to individual constituent processes. How does a hypothesis that exists at this level survive in a scientific community driven first and foremost by reductionism and demands silver-bullet solutions to neurodegenerative disorders? Practically, what empirical data would prove the necessity of a systems-level perspective over a reductionistic one? To ask this question another way, given the multiple levels at which a problem can be studied (e.g., in neuroscience: organismal > systems > cellular > molecular > genetic) is there a general approach to empirically establish the level at which a phenomenon of interest (e.g., Alzheimer’s disease) is most clearly resolved? If functional failure were proven to result from systems-level degeneration without clear links to individual constituent processes, thus making individual molecular targets tangentially relevant, what treatment approaches hold the greatest promise? </div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Location=Santa Fe Institute</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Location=Santa Fe Institute</div></td></tr>
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</table>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Cognitive_Regime_Shift_II_-_When/why/how_the_Brain_Breaks&diff=5054&oldid=prevAmyPChen at 18:40, November 11, 20192019-11-11T18:40:48Z<p></p>
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 18:40, November 11, 2019</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l19" >Line 19:</td>
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<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* John Krakauer: Network approaches are largely anti-modular and atheoretical. There seems to be a tension between conceiving the brain as computationally/algorithmically modular but implementationally distributed at least when it comes to cognition in cortex. The mapping between these two tends to consist of correlations between network metrics and task/behavioral variables. It is not clear how informative this is. Is it?</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* John Krakauer: Network approaches are largely anti-modular and atheoretical. There seems to be a tension between conceiving the brain as computationally/algorithmically modular but implementationally distributed at least when it comes to cognition in cortex. The mapping between these two tends to consist of correlations between network metrics and task/behavioral variables. It is not clear how informative this is. Is it?</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* Jack Gallant: (1) All models of human brain function are fundamentally limited by the sensitivity of brain measurement devices, the number of stimulus and task conditions sampled in a study, and the number of and types of individuals sampled. Given these constraints, how can we optimize experimental design and modeling so as to produce medically relevant and actionable information for individuals? (2) Currently most models of the human brain have only been validated in terms of statistical significance at the group level. Few current models provide individualized predictions, and fewer still test generalization outside the conditions used to fit the model. How well does a model have to predict and generalize to an individual's daily life before it is useful for medicine and for other applications?</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* Jack Gallant: (1) All models of human brain function are fundamentally limited by the sensitivity of brain measurement devices, the number of stimulus and task conditions sampled in a study, and the number of and types of individuals sampled. Given these constraints, how can we optimize experimental design and modeling so as to produce medically relevant and actionable information for individuals? (2) Currently most models of the human brain have only been validated in terms of statistical significance at the group level. Few current models provide individualized predictions, and fewer still test generalization outside the conditions used to fit the model. How well does a model have to predict and generalize to an individual's daily life before it is useful for medicine and for other applications?</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div><del style="font-weight: bold; text-decoration: none;">* Danielle S. Bassett: (1) In relation to Braun et al. 2019 - How do energetic constraints impinge on other cognitive functions? Does the energy landscape change over neurodevelopment in a manner that tracks the onset and progression of disease? What is the information content of these states, and how does energy depend on information? (2) In relation to Lynn et al. 2019 - How does disease alter perceived information in the world around us? What neurophysiological substrates might explain that alteration? Can we circumvent human biases in perception by restructuring information?</del></div></td><td colspan="2"> </td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* Caterina Gratton: Most fMRI studies (in the domain of aging as well as healthy young adults) find only relatively small relationships between brain measures and behavior. What theories or methods can we develop to improve this link?</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* Caterina Gratton: Most fMRI studies (in the domain of aging as well as healthy young adults) find only relatively small relationships between brain measures and behavior. What theories or methods can we develop to improve this link?</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* Paul Garcia: Temporal judgment can be altered during sleep, anesthesia, meditation, and mind-wander. What is the relationship between time perception, attention, and consciousness? Since working memory is often affected in delirium and dementia, is a broken brain unable to recognize mind wander? As we age do we become more self-reflective or less? What are the roles of volition, sentience, and agency in experiencing time? Is temporal judgment a uniquely human phenomenon? </div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* Paul Garcia: Temporal judgment can be altered during sleep, anesthesia, meditation, and mind-wander. What is the relationship between time perception, attention, and consciousness? Since working memory is often affected in delirium and dementia, is a broken brain unable to recognize mind wander? As we age do we become more self-reflective or less? What are the roles of volition, sentience, and agency in experiencing time? Is temporal judgment a uniquely human phenomenon? </div></td></tr>
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<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* Ehren Newman: Taking seriously the idea that complex systems exist in their own right leads to the idea that functional failure can result from degeneration at the systems-level without clear connection to individual constituent processes. How does a hypothesis that exists at this level survive in a scientific community driven first and foremost by reductionism and demands silver-bullet solutions to neurodegenerative disorders? Practically, what empirical data would prove the necessity of a systems-level perspective over a reductionistic one? To ask this question another way, given the multiple levels at which a problem can be studied (e.g., in neuroscience: organismal > systems > cellular > molecular > genetic) is there a general approach to empirically establish the level at which a phenomenon of interest (e.g., Alzheimer’s disease) is most clearly resolved? If functional failure were proven to result from systems-level degeneration without clear links to individual constituent processes, thus making individual molecular targets tangentially relevant, what treatment approaches hold the greatest promise? </div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* Ehren Newman: Taking seriously the idea that complex systems exist in their own right leads to the idea that functional failure can result from degeneration at the systems-level without clear connection to individual constituent processes. How does a hypothesis that exists at this level survive in a scientific community driven first and foremost by reductionism and demands silver-bullet solutions to neurodegenerative disorders? Practically, what empirical data would prove the necessity of a systems-level perspective over a reductionistic one? To ask this question another way, given the multiple levels at which a problem can be studied (e.g., in neuroscience: organismal > systems > cellular > molecular > genetic) is there a general approach to empirically establish the level at which a phenomenon of interest (e.g., Alzheimer’s disease) is most clearly resolved? If functional failure were proven to result from systems-level degeneration without clear links to individual constituent processes, thus making individual molecular targets tangentially relevant, what treatment approaches hold the greatest promise? </div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Location=Santa Fe Institute</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|Location=Santa Fe Institute</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>|Attendee list=JacopoGrilli;CaterinaGratton;DietmarPlenz;SusanFitzpatrick<del class="diffchange diffchange-inline">;DanielleBassett</del>;RobertoCabeza;JackGallant;RussPoldrack;PaulGarcia;RandyMcIntosh;ViktorJirsa;RichardFrackowiak;NikolausKriegeskorte;SidneyRedner;NihatAy;Ehren Newman;Guy Miller</div></td><td class='diff-marker'>+</td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>|Attendee list=JacopoGrilli;CaterinaGratton;DietmarPlenz;SusanFitzpatrick;RobertoCabeza;JackGallant;RussPoldrack;PaulGarcia;RandyMcIntosh;ViktorJirsa;RichardFrackowiak;NikolausKriegeskorte;SidneyRedner;NihatAy;Ehren Newman;Guy Miller</div></td></tr>
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</table>AmyPChen