https://centre.santafe.edu/complextime/w/api.php?action=feedcontributions&user=AmyPChen&feedformat=atomComplex Time - User contributions [en]2024-03-28T10:49:40ZUser contributionsMediaWiki 1.35.6https://centre.santafe.edu/complextime/w/index.php?title=User:SrividyaIyer-Biswas&diff=5580User:SrividyaIyer-Biswas2021-04-28T04:34:21Z<p>AmyPChen: </p>
<hr />
<div>{{Researcher<br />
|Image=Sri Iyer-biswas.jpeg<br />
|Name=Srividya Iyer-Biswas<br />
|Affiliation=Purdue Univ./SFI<br />
|Email address=iyerbiswas@purdue.edu<br />
|Related links={{Related link<br />
|Related link title=Iyer-Biswas Lab<br />
|Related link URL=http://iyerbiswas.com/<br />
}}<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=File:SFIPilotBirthDeathAging_Nov24_ABaudisch.pptx&diff=5575File:SFIPilotBirthDeathAging Nov24 ABaudisch.pptx2021-04-23T19:38:36Z<p>AmyPChen: User created page with UploadWizard</p>
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[[Category:Uploaded via Campaign:Presentation file]]</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Toward_a_multi-scale_theory_of_birth_and_death_pattern/Toward_a_multi-scale_theory_of_birth_and_death_patterns&diff=5574Toward a multi-scale theory of birth and death pattern/Toward a multi-scale theory of birth and death patterns2021-04-23T19:37:28Z<p>AmyPChen: Created page with "{{Agenda item |Start time=November 24, 2020 10:30:00 AM |End time=November 24, 2020 11:30:00 AM |Is presentation=No |Presenter=Annette Baudisch }}"</p>
<hr />
<div>{{Agenda item<br />
|Start time=November 24, 2020 10:30:00 AM<br />
|End time=November 24, 2020 11:30:00 AM<br />
|Is presentation=No<br />
|Presenter=Annette Baudisch<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=File:WhatisDying_DK.pdf&diff=5573File:WhatisDying DK.pdf2021-04-23T19:34:50Z<p>AmyPChen: User created page with UploadWizard</p>
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|description={{Presentation file for|Toward a multi-scale theory of birth and death pattern/What is aging &#38; what is dying?}}{{Presentation file for presenter|David Krakauer}}<br />
|date=<br />
|source={{own}}<br />
|author=[[User:AmyPChen|AmyPChen]]<br />
|permission=<br />
|other versions=<br />
}}<br />
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<br />
[[Category:Uploaded via Campaign:Presentation file]]</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Toward_a_multi-scale_theory_of_birth_and_death_pattern/What_is_aging_%26_what_is_dying%3F&diff=5572Toward a multi-scale theory of birth and death pattern/What is aging & what is dying?2021-04-23T19:30:51Z<p>AmyPChen: Created page with "{{Agenda item |Start time=November 24, 2020 09:30:00 AM |End time=November 24, 2020 10:30:00 AM |Is presentation=No |Presenter=DavidKrakauer }}"</p>
<hr />
<div>{{Agenda item<br />
|Start time=November 24, 2020 09:30:00 AM<br />
|End time=November 24, 2020 10:30:00 AM<br />
|Is presentation=No<br />
|Presenter=DavidKrakauer<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Toward_a_multi-scale_theory_of_birth_and_death_pattern/Round-table_introduction&diff=5571Toward a multi-scale theory of birth and death pattern/Round-table introduction2021-04-23T19:29:53Z<p>AmyPChen: Created page with "{{Agenda item |Start time=November 24, 2020 09:00:00 AM |End time=November 24, 2020 09:30:00 AM |Is presentation=No |Presenter=DavidKrakauer }}"</p>
<hr />
<div>{{Agenda item<br />
|Start time=November 24, 2020 09:00:00 AM<br />
|End time=November 24, 2020 09:30:00 AM<br />
|Is presentation=No<br />
|Presenter=DavidKrakauer<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Toward_a_multi-scale_theory_of_birth_and_death_pattern&diff=5570Toward a multi-scale theory of birth and death pattern2021-04-23T19:28:14Z<p>AmyPChen: </p>
<hr />
<div>{{Meeting<br />
|Type of meeting=Core Theory<br />
|Start date/time=November 24, 2020<br />
|End date/time=January 4, 2021<br />
|Organizers=DavidKrakauer;Annette Baudisch<br />
|Meeting summary=In this meeting on approaches to a multi-scale theory of birth and death patterns we are convening a small and informal group to discuss both the scope of a new application area in the JSMF funded Complex Time research theme as well as identifying key individuals we would like to become involved. We seek to identify diverse expertise in order to integrate birth-development-death concepts across a broad range of adaptive scales. The meeting is centered around four basic questions: (1) how best to conceptualize the individual? (2) how and why individuals age (3) how models should vary as a function of application domain (e.g. biology or culture) and (4) how we might parameterize universal patterns of aging.<br />
|Location=By Zoom<br />
|Attendee list=SrividyaIyer-Biswas;ChrisKempes;GeoffreyWest;DougErwin;Venki Ramakrishnan<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Complex_Time:Home/Slideshow&diff=5569Complex Time:Home/Slideshow2021-04-22T21:19:43Z<p>AmyPChen: </p>
<hr />
<div>{{Slideshow<br />
|Slides={{Slide<br />
|Image=Birth Death Slideshow Image.jpg<br />
|Heading=Core Theory Meeting: Toward a multi-scale theory of birth and death pattern<br />
|Link=https://centre.santafe.edu/complextime/Toward_a_multi-scale_theory_of_birth_and_death_pattern<br />
|Text=November 24, 2020; birth and death patterns for individuals, institutions, culture, etc.<br />
}}{{Slide<br />
|Image=Single Cell.png<br />
|Heading=Working Group: Aging in single-celled organisms: from bacteria to the whole tree of life<br />
|Link=https://centre.santafe.edu/complextime/Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life<br />
|Text=February 10-12, 2020; What are the processes & implications of how single-celled organisms age?<br />
}}{{Slide}}<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=File:Birth_Death_Slideshow_Image.jpg&diff=5568File:Birth Death Slideshow Image.jpg2021-04-22T18:49:37Z<p>AmyPChen: </p>
<hr />
<div></div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Complex_Time:Home/Slideshow&diff=5567Complex Time:Home/Slideshow2021-04-22T18:39:19Z<p>AmyPChen: </p>
<hr />
<div>{{Slideshow<br />
|Slides={{Slide<br />
|Image=Tolga-ulkan-9k36QqhA0cU-unsplash.jpg<br />
|Heading=Core Theory Meeting: Toward a multi-scale theory of birth and death pattern<br />
|Link=https://centre.santafe.edu/complextime/Toward_a_multi-scale_theory_of_birth_and_death_pattern<br />
|Text=November 24, 2020; birth and death patterns for individuals, institutions, culture, etc.<br />
}}{{Slide<br />
|Image=Single Cell.png<br />
|Heading=Working Group: Aging in single-celled organisms: from bacteria to the whole tree of life<br />
|Link=https://centre.santafe.edu/complextime/Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life<br />
|Text=February 10-12, 2020; What are the processes & implications of how single-celled organisms age?<br />
}}{{Slide}}<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=File:Tolga-ulkan-9k36QqhA0cU-unsplash.jpg&diff=5566File:Tolga-ulkan-9k36QqhA0cU-unsplash.jpg2021-04-22T18:34:30Z<p>AmyPChen: </p>
<hr />
<div></div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Toward_a_multi-scale_theory_of_birth_and_death_pattern&diff=5549Toward a multi-scale theory of birth and death pattern2020-11-10T22:50:13Z<p>AmyPChen: </p>
<hr />
<div>{{Meeting<br />
|Type of meeting=Core Theory<br />
|Start date/time=November 24, 2020<br />
|End date/time=November 24, 2020<br />
|Organizers=DavidKrakauer;Annette Baudisch<br />
|Meeting summary=In this meeting on approaches to a multi-scale theory of birth and death patterns we are convening a small and informal group to discuss both the scope of a new application area in the JSMF funded Complex Time research theme as well as identifying key individuals we would like to become involved. We seek to identify diverse expertise in order to integrate birth-development-death concepts across a broad range of adaptive scales. The meeting is centered around four basic questions: (1) how best to conceptualize the individual? (2) how and why individuals age (3) how models should vary as a function of application domain (e.g. biology or culture) and (4) how we might parameterize universal patterns of aging.<br />
|Location=By Zoom<br />
|Attendee list=SrividyaIyer-Biswas;ChrisKempes;GeoffreyWest;DougErwin;Venki Ramakrishnan<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Toward_a_multi-scale_theory_of_birth_and_death_pattern&diff=5537Toward a multi-scale theory of birth and death pattern2020-10-27T20:30:14Z<p>AmyPChen: </p>
<hr />
<div>{{Meeting<br />
|Type of meeting=Core Theory<br />
|Start date/time=November 24, 2020<br />
|End date/time=November 24, 2020<br />
|Organizers=DavidKrakauer<br />
|Meeting summary=In this meeting on approaches to a multi-scale theory of birth and death patterns we are convening a small and informal group to discuss both the scope of a new application area in the JSMF funded Complex Time research theme as well as identifying key individuals we would like to become involved. We seek to identify diverse expertise in order to integrate birth-development-death concepts across a broad range of adaptive scales. The meeting is centered around four basic questions: (1) how best to conceptualize the individual? (2) how and why individuals age (3) how models should vary as a function of application domain (e.g. biology or culture) and (4) how we might parameterize universal patterns of aging.<br />
|Location=By Zoom<br />
|Attendee list=SrividyaIyer-Biswas;ChrisKempes;GeoffreyWest;DougErwin<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Toward_a_multi-scale_theory_of_birth_and_death_pattern&diff=5533Toward a multi-scale theory of birth and death pattern2020-10-20T20:18:48Z<p>AmyPChen: Created page with "{{Meeting |Type of meeting=Core Theory |Start date/time=November 24, 2020 |End date/time=November 24, 2020 |Organizers=DavidKrakauer |Meeting summary=In this meeting on approa..."</p>
<hr />
<div>{{Meeting<br />
|Type of meeting=Core Theory<br />
|Start date/time=November 24, 2020<br />
|End date/time=November 24, 2020<br />
|Organizers=DavidKrakauer<br />
|Meeting summary=In this meeting on approaches to a multi-scale theory of birth and death patterns we are convening a small and informal group to discuss both the scope of a new application area in the JSMF funded Complex Time research theme as well as identifying key individuals we would like to become involved. We seek to identify diverse expertise in order to integrate birth-development-death concepts across a broad range of adaptive scales. The meeting is centered around four basic questions: (1) how best to conceptualize the individual? (2) how and why individuals age (3) how models should vary as a function of application domain (e.g. biology or culture) and (4) how we might parameterize universal patterns of aging.<br />
|Location=By Zoom<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Cognitive_Regime_Shift_II_-_When/why/how_the_Brain_Breaks&diff=5531Cognitive Regime Shift II - When/why/how the Brain Breaks2020-05-21T20:47:21Z<p>AmyPChen: </p>
<hr />
<div>{{Meeting<br />
|Type of meeting=Application Area<br />
|Application area=Aging Brain<br />
|Start date/time=November 12, 2019<br />
|End date/time=November 13, 2019<br />
|Meeting video=https://www.youtube.com/watch?v=TwL5IMkNrwk&list=PLZlVBTf7N6GoAPu-80tFHGLD39e3uidj3&index=13<br />
|Organizers=StevenPetersen;DavidKrakauer;JohnKrakauer<br />
|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. <br />
|Additional info=We will model the format of this WG loosely after the successful Dahlem Konferenzen. In preparation, we ask everyone to please (1) nominate one or two reference(s) bearing on the WG synopsis (with a note on why you chose each), and (2) come up with one or two question(s) that you would like to discuss with the group at the meeting. <br />
<br />
'''Questions:'''<br />
* David Krakauer: What is the connection of physiological robustness in the nervous system (why brains do not break) to the information processing, computational, or functional properties of the brain? In other words are diseases of the brain deficits of information processing or general injuries shared across any densely connected tissues or organ?<br />
* Russ Poldrack: There are currently two very different approaches to understanding brain networks, which have very different implications for the impact of damage to the network. One approach, which arises from computational neuroscience, has focused on the nature of the computations that are performed by specific brain circuits or regions. This approach is well exemplified by the recent work from Yamins, DiCarlo, and others that has used task-driven neural network models to predict neuronal signals. A second approach, which falls under the blanket term of “network neuroscience”, has applied generic methods for understanding networks and complex systems. Whereas the former approach focuses on the differences in the kinds of computations that are performed by different networks, the latter largely treats the function of the individual network elements as interchangeable - for example, graph theoretic methods that characterize function in terms of concepts such as path length generally do not care which specific nodes fall on the potential paths. Understanding the effects of damage on neural computational will almost certainly require an understanding of how to integrate these two perspectives, and the people at this meeting are well placed to think about this issue.<br />
* Richard Frackowiak: (1) For clinicians the value of a generalised model is measured by its utility in individuals. If a neuroscientist claims a lucid theory of the function of some aspect of the brain is explanatory, because it fits a model with half a dozen dimensions derived from fifty people, what do we tell patients if the model does not fit their data and fails in prognostic prediction? That they are noise, or perhaps suffer from a defect of some other function? These would be acceptable answers only if more complex models showed inferior predictive power, then the unmodelled variance would indeed plausibly represent noise. Once a model with better and more generalisable predictive power is found, what was previously considered noise is now explained. Should the resultant complexity of the explanation (not intuitively understandable) be a barrier to its utility? Clinically, generalisable individual predictive performance always trumps lucidity. Shouldn’t the clinician’s primary concern be the scientist's too? (2) To understand where the brain breaks and how to treat it when it breaks we will need high resolution views of all aspects of the brain - maps and models relating everything - but we keep skirting this necessity. Have advances in data management and analytical informatics resulted in a radical change in the scientific method through an ability to generate hypotheses from data rather than by the intuition of illuminated individuals. Is this a true statement at the current state of play? Is a “theory of the brain” a realisable project and if so, how would it help the understanding of brain breakdown in psychiatric and neurodegenerative disorders? Though an initial aspiration of the EU’s Human Brain Project, that focus has dissipated but remains a challenge for a few laboratories. Is reigniting this ambition massively a realisable priority for those interested in understanding the complex organisation of the human brain and how it responds to injury and degeneration? A further major challenge is for scientists to understand the issues faced by clinicians more deeply. <br />
* Roberto Cabeza: How does the concept of robustness relate to the concepts of reserve, maintenance, and compensation in the domains of aging, dementia, and brain damage?<br />
* Viktor Jirsa: What is information processing in an oscillatory network and how does it link to human behavior? Said differently, in brain disease, why do certain parameter changes of the brain network sometimes affect human behavior and sometimes leave it untouched?<br />
* Randy McIntosh: Can we find a way to make a principled distinction between clinical deficits are come from 1) uncovering a hidden capacity of the system, 2) a maladaptive response to injury/disease, or 3) a primary response to loss (e.g., focal lesion)?<br />
* Susan Fitzpatrick: There has been a tendency to over-constrain the way we study neurological disorders- influenced in part by the molecular revolution. The risk of such approaches is that identified and over- targeted local perturbations that become the focus of searches for treatment might not matter (and certainly not “fix” ) because of adaptations such that circuits and networks remain functional. Until of course, they have moved further and further from a healthy state that the cliff looms. Targeting networks as the level of intervention using very crude approaches could actually have ameliorative effects (think ketogenic diet for epilepsy) but might lead to a different dilemma – under-constraining our knowledge and impeding progress. How do we get the size of the space for intervening in complex adaptive systems “right?” <br />
* Jacopo Grilli: Do brains break in the same way? From the theory of large deviations, we know that very rare events are likely to occur consistently in the same way. If aging and neurological disorders are the results of a regime shift, how many regimes there are? Two or many? How does this depend on the level of coarse-graining? How much are the transitions between these regimes replicable?<br />
* 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?<br />
* 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?<br />
* 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?<br />
* 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? <br />
* Dietmar Plenz: Does normal brain function during wakefulness equate with a single dynamical state, e.g. critical dynamics, from where diseases explore mutually orthogonal, low-dimensional trajectory away from this state?<br />
* Steve Petersen: Will resting state correlations be useful for understanding complex systems effects in neurodegenerative disease?<br />
* Artemy Kolchinsky: The brain exhibits both redundancy (some functions can be interchangeably carried out by different components) and synergy (some functions require multiple components to operate in a coordinated manner). It is unclear how to assign functions to individual components in the presence of redundancy and synergy. How (and why) does the level of redundancy and synergy in the brain differ in comparison to other biological and technological systems? Does it change as we consider the brain at different scales? Does the level of redundancy and synergy characterize how a system will ultimately fail? <br />
* 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? <br />
|Location=Santa Fe Institute<br />
|Attendee list=JacopoGrilli;CaterinaGratton;DietmarPlenz;SusanFitzpatrick;RobertoCabeza;JackGallant;RussPoldrack;PaulGarcia;RandyMcIntosh;ViktorJirsa;RichardFrackowiak;NikolausKriegeskorte;SidneyRedner;NihatAy;Ehren Newman;GuyMiller;Tyler Marghetis;ArtemyKolchinsky<br />
|Post-meeting summary=Coming soon.<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Cognitive_Regime_Shift_II_-_When/why/how_the_Brain_Breaks&diff=5530Cognitive Regime Shift II - When/why/how the Brain Breaks2020-05-21T20:43:58Z<p>AmyPChen: </p>
<hr />
<div>{{Meeting<br />
|Type of meeting=Application Area<br />
|Application area=Aging Brain<br />
|Start date/time=November 12, 2019<br />
|End date/time=November 13, 2019<br />
|Meeting video=https://youtu.be/TwL5IMkNrwk<br />
|Organizers=StevenPetersen;DavidKrakauer;JohnKrakauer<br />
|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. <br />
|Additional info=We will model the format of this WG loosely after the successful Dahlem Konferenzen. In preparation, we ask everyone to please (1) nominate one or two reference(s) bearing on the WG synopsis (with a note on why you chose each), and (2) come up with one or two question(s) that you would like to discuss with the group at the meeting. <br />
<br />
'''Questions:'''<br />
* David Krakauer: What is the connection of physiological robustness in the nervous system (why brains do not break) to the information processing, computational, or functional properties of the brain? In other words are diseases of the brain deficits of information processing or general injuries shared across any densely connected tissues or organ?<br />
* Russ Poldrack: There are currently two very different approaches to understanding brain networks, which have very different implications for the impact of damage to the network. One approach, which arises from computational neuroscience, has focused on the nature of the computations that are performed by specific brain circuits or regions. This approach is well exemplified by the recent work from Yamins, DiCarlo, and others that has used task-driven neural network models to predict neuronal signals. A second approach, which falls under the blanket term of “network neuroscience”, has applied generic methods for understanding networks and complex systems. Whereas the former approach focuses on the differences in the kinds of computations that are performed by different networks, the latter largely treats the function of the individual network elements as interchangeable - for example, graph theoretic methods that characterize function in terms of concepts such as path length generally do not care which specific nodes fall on the potential paths. Understanding the effects of damage on neural computational will almost certainly require an understanding of how to integrate these two perspectives, and the people at this meeting are well placed to think about this issue.<br />
* Richard Frackowiak: (1) For clinicians the value of a generalised model is measured by its utility in individuals. If a neuroscientist claims a lucid theory of the function of some aspect of the brain is explanatory, because it fits a model with half a dozen dimensions derived from fifty people, what do we tell patients if the model does not fit their data and fails in prognostic prediction? That they are noise, or perhaps suffer from a defect of some other function? These would be acceptable answers only if more complex models showed inferior predictive power, then the unmodelled variance would indeed plausibly represent noise. Once a model with better and more generalisable predictive power is found, what was previously considered noise is now explained. Should the resultant complexity of the explanation (not intuitively understandable) be a barrier to its utility? Clinically, generalisable individual predictive performance always trumps lucidity. Shouldn’t the clinician’s primary concern be the scientist's too? (2) To understand where the brain breaks and how to treat it when it breaks we will need high resolution views of all aspects of the brain - maps and models relating everything - but we keep skirting this necessity. Have advances in data management and analytical informatics resulted in a radical change in the scientific method through an ability to generate hypotheses from data rather than by the intuition of illuminated individuals. Is this a true statement at the current state of play? Is a “theory of the brain” a realisable project and if so, how would it help the understanding of brain breakdown in psychiatric and neurodegenerative disorders? Though an initial aspiration of the EU’s Human Brain Project, that focus has dissipated but remains a challenge for a few laboratories. Is reigniting this ambition massively a realisable priority for those interested in understanding the complex organisation of the human brain and how it responds to injury and degeneration? A further major challenge is for scientists to understand the issues faced by clinicians more deeply. <br />
* Roberto Cabeza: How does the concept of robustness relate to the concepts of reserve, maintenance, and compensation in the domains of aging, dementia, and brain damage?<br />
* Viktor Jirsa: What is information processing in an oscillatory network and how does it link to human behavior? Said differently, in brain disease, why do certain parameter changes of the brain network sometimes affect human behavior and sometimes leave it untouched?<br />
* Randy McIntosh: Can we find a way to make a principled distinction between clinical deficits are come from 1) uncovering a hidden capacity of the system, 2) a maladaptive response to injury/disease, or 3) a primary response to loss (e.g., focal lesion)?<br />
* Susan Fitzpatrick: There has been a tendency to over-constrain the way we study neurological disorders- influenced in part by the molecular revolution. The risk of such approaches is that identified and over- targeted local perturbations that become the focus of searches for treatment might not matter (and certainly not “fix” ) because of adaptations such that circuits and networks remain functional. Until of course, they have moved further and further from a healthy state that the cliff looms. Targeting networks as the level of intervention using very crude approaches could actually have ameliorative effects (think ketogenic diet for epilepsy) but might lead to a different dilemma – under-constraining our knowledge and impeding progress. How do we get the size of the space for intervening in complex adaptive systems “right?” <br />
* Jacopo Grilli: Do brains break in the same way? From the theory of large deviations, we know that very rare events are likely to occur consistently in the same way. If aging and neurological disorders are the results of a regime shift, how many regimes there are? Two or many? How does this depend on the level of coarse-graining? How much are the transitions between these regimes replicable?<br />
* 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?<br />
* 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?<br />
* 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?<br />
* 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? <br />
* Dietmar Plenz: Does normal brain function during wakefulness equate with a single dynamical state, e.g. critical dynamics, from where diseases explore mutually orthogonal, low-dimensional trajectory away from this state?<br />
* Steve Petersen: Will resting state correlations be useful for understanding complex systems effects in neurodegenerative disease?<br />
* Artemy Kolchinsky: The brain exhibits both redundancy (some functions can be interchangeably carried out by different components) and synergy (some functions require multiple components to operate in a coordinated manner). It is unclear how to assign functions to individual components in the presence of redundancy and synergy. How (and why) does the level of redundancy and synergy in the brain differ in comparison to other biological and technological systems? Does it change as we consider the brain at different scales? Does the level of redundancy and synergy characterize how a system will ultimately fail? <br />
* 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? <br />
|Location=Santa Fe Institute<br />
|Attendee list=JacopoGrilli;CaterinaGratton;DietmarPlenz;SusanFitzpatrick;RobertoCabeza;JackGallant;RussPoldrack;PaulGarcia;RandyMcIntosh;ViktorJirsa;RichardFrackowiak;NikolausKriegeskorte;SidneyRedner;NihatAy;Ehren Newman;GuyMiller;Tyler Marghetis;ArtemyKolchinsky<br />
|Post-meeting summary=Coming soon.<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life&diff=5525Aging in Single-celled Organisms: from Bacteria to the Whole Tree of Life2020-05-14T22:16:51Z<p>AmyPChen: </p>
<hr />
<div>{{Meeting<br />
|Type of meeting=Application Area<br />
|Application area=Cellular Aging<br />
|Start date/time=February 10, 2020<br />
|End date/time=February 12, 2020<br />
|Meeting video=https://www.youtube.com/watch?v=2IZjde0D6Gw&feature=youtu.be<br />
|Organizers=JacopoGrilli;ChrisKempes;MatteoOsella;SrividyaIyer-Biswas<br />
|Meeting summary=This working group will bring together experimentalists and theoreticians to better understand the processes and implications of how single-celled organisms age. General principles will be drawn from high-throughput growth and division data of aging single-cells. Energetics by which they store and process information will be connected with those in larger, multicellular organisms. Some key questions this working group will consider include how the aging clock in a single-celled organism is coupled to that of a more complex organism in which it resides (and vise versa), how aging changes with growth and division, how cells with different age process information differently from the environment, and how aging differ across the tree of life. <br />
|Attendee list=MartinPicard;UliSteiner;SabrinaSpencer;LinChao;VanSavage;Bree Aldridge;Owen Jones;GeoffreyWest<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Aging_and_Adaptation_in_Infectious_Diseases_III&diff=5524Aging and Adaptation in Infectious Diseases III2020-05-14T22:16:14Z<p>AmyPChen: </p>
<hr />
<div>{{Meeting<br />
|Type of meeting=Application Area<br />
|Application area=Infectious Diseases<br />
|Start date/time=January 14, 2020<br />
|End date/time=January 17, 2020<br />
|Meeting video=https://www.youtube.com/watch?v=LMDLuKgmfK0&feature=youtu.be<br />
|Organizers=MercedesPascual;JeanCarlson<br />
|Meeting summary=Our working group aims to explore the role of aging and adaptation in infectious diseases operating over multiple organizational and temporal scales. General areas include immune system dynamics and age, host-pathogen co-adaptation in chronic vs. acute infections, pathogen antigenic diversity and endemism, effects of age on infectious diseases in human and non-human hosts. Overarching themes include memory, (co)adaptation, diversity, feedback, robustness and fragility. We are interested in aging as increasing fragility to infection, and in complex biological time as related to individual variation in disease progression and recovery. We are also interested in aging of the pathogen in terms of its ability to persist and withstand intervention efforts, and how this robustness is in turn related to pathogen (antigenic) diversity. In all these areas, the dynamic acquisition and loss of information through the immune system plays a central role at the individual and population levels. The goal of this third working group is to reunite participants from the first and second meetings to update progress and develop our next set of objectives for collaborative research on the questions that emerged from our previous discussions. These questions include the interaction of the adaptive and innate immune system in the dynamics of infection, the role of early-childhood exposure (‘imprinting’) in later immune protection and in defining the temporal changes of the antigenic map, and the allometric scaling of the immune system dynamics with organism size.<br />
|Location=Santa Fe Institute (Noyce Conference Room)<br />
|Attendee list=SarahCobey;AndrewPDobson;AndreaLGraham;KatiaKoelle;MicaelaMartinez;AlanPerelson;DavidSchneider;ShenshenWang;JimingSheng;MarcosViera;EricJones;KatieGostic;PhilArevalo;PamelaMartinez;Qixin He;Kangchon Kim<br />
}}<br />
[[Category:Agenda meetings]]</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Cognitive_Regime_Shift_II_-_When/why/how_the_Brain_Breaks&diff=5523Cognitive Regime Shift II - When/why/how the Brain Breaks2020-05-14T22:11:08Z<p>AmyPChen: </p>
<hr />
<div>{{Meeting<br />
|Type of meeting=Application Area<br />
|Application area=Aging Brain<br />
|Start date/time=November 12, 2019<br />
|End date/time=November 13, 2019<br />
|Meeting video=https://www.youtube.com/watch?v=HnA91mymghA&feature=youtu.be<br />
|Organizers=StevenPetersen;DavidKrakauer;JohnKrakauer<br />
|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. <br />
|Additional info=We will model the format of this WG loosely after the successful Dahlem Konferenzen. In preparation, we ask everyone to please (1) nominate one or two reference(s) bearing on the WG synopsis (with a note on why you chose each), and (2) come up with one or two question(s) that you would like to discuss with the group at the meeting. <br />
<br />
'''Questions:'''<br />
* David Krakauer: What is the connection of physiological robustness in the nervous system (why brains do not break) to the information processing, computational, or functional properties of the brain? In other words are diseases of the brain deficits of information processing or general injuries shared across any densely connected tissues or organ?<br />
* Russ Poldrack: There are currently two very different approaches to understanding brain networks, which have very different implications for the impact of damage to the network. One approach, which arises from computational neuroscience, has focused on the nature of the computations that are performed by specific brain circuits or regions. This approach is well exemplified by the recent work from Yamins, DiCarlo, and others that has used task-driven neural network models to predict neuronal signals. A second approach, which falls under the blanket term of “network neuroscience”, has applied generic methods for understanding networks and complex systems. Whereas the former approach focuses on the differences in the kinds of computations that are performed by different networks, the latter largely treats the function of the individual network elements as interchangeable - for example, graph theoretic methods that characterize function in terms of concepts such as path length generally do not care which specific nodes fall on the potential paths. Understanding the effects of damage on neural computational will almost certainly require an understanding of how to integrate these two perspectives, and the people at this meeting are well placed to think about this issue.<br />
* Richard Frackowiak: (1) For clinicians the value of a generalised model is measured by its utility in individuals. If a neuroscientist claims a lucid theory of the function of some aspect of the brain is explanatory, because it fits a model with half a dozen dimensions derived from fifty people, what do we tell patients if the model does not fit their data and fails in prognostic prediction? That they are noise, or perhaps suffer from a defect of some other function? These would be acceptable answers only if more complex models showed inferior predictive power, then the unmodelled variance would indeed plausibly represent noise. Once a model with better and more generalisable predictive power is found, what was previously considered noise is now explained. Should the resultant complexity of the explanation (not intuitively understandable) be a barrier to its utility? Clinically, generalisable individual predictive performance always trumps lucidity. Shouldn’t the clinician’s primary concern be the scientist's too? (2) To understand where the brain breaks and how to treat it when it breaks we will need high resolution views of all aspects of the brain - maps and models relating everything - but we keep skirting this necessity. Have advances in data management and analytical informatics resulted in a radical change in the scientific method through an ability to generate hypotheses from data rather than by the intuition of illuminated individuals. Is this a true statement at the current state of play? Is a “theory of the brain” a realisable project and if so, how would it help the understanding of brain breakdown in psychiatric and neurodegenerative disorders? Though an initial aspiration of the EU’s Human Brain Project, that focus has dissipated but remains a challenge for a few laboratories. Is reigniting this ambition massively a realisable priority for those interested in understanding the complex organisation of the human brain and how it responds to injury and degeneration? A further major challenge is for scientists to understand the issues faced by clinicians more deeply. <br />
* Roberto Cabeza: How does the concept of robustness relate to the concepts of reserve, maintenance, and compensation in the domains of aging, dementia, and brain damage?<br />
* Viktor Jirsa: What is information processing in an oscillatory network and how does it link to human behavior? Said differently, in brain disease, why do certain parameter changes of the brain network sometimes affect human behavior and sometimes leave it untouched?<br />
* Randy McIntosh: Can we find a way to make a principled distinction between clinical deficits are come from 1) uncovering a hidden capacity of the system, 2) a maladaptive response to injury/disease, or 3) a primary response to loss (e.g., focal lesion)?<br />
* Susan Fitzpatrick: There has been a tendency to over-constrain the way we study neurological disorders- influenced in part by the molecular revolution. The risk of such approaches is that identified and over- targeted local perturbations that become the focus of searches for treatment might not matter (and certainly not “fix” ) because of adaptations such that circuits and networks remain functional. Until of course, they have moved further and further from a healthy state that the cliff looms. Targeting networks as the level of intervention using very crude approaches could actually have ameliorative effects (think ketogenic diet for epilepsy) but might lead to a different dilemma – under-constraining our knowledge and impeding progress. How do we get the size of the space for intervening in complex adaptive systems “right?” <br />
* Jacopo Grilli: Do brains break in the same way? From the theory of large deviations, we know that very rare events are likely to occur consistently in the same way. If aging and neurological disorders are the results of a regime shift, how many regimes there are? Two or many? How does this depend on the level of coarse-graining? How much are the transitions between these regimes replicable?<br />
* 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?<br />
* 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?<br />
* 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?<br />
* 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? <br />
* Dietmar Plenz: Does normal brain function during wakefulness equate with a single dynamical state, e.g. critical dynamics, from where diseases explore mutually orthogonal, low-dimensional trajectory away from this state?<br />
* Steve Petersen: Will resting state correlations be useful for understanding complex systems effects in neurodegenerative disease?<br />
* Artemy Kolchinsky: The brain exhibits both redundancy (some functions can be interchangeably carried out by different components) and synergy (some functions require multiple components to operate in a coordinated manner). It is unclear how to assign functions to individual components in the presence of redundancy and synergy. How (and why) does the level of redundancy and synergy in the brain differ in comparison to other biological and technological systems? Does it change as we consider the brain at different scales? Does the level of redundancy and synergy characterize how a system will ultimately fail? <br />
* 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? <br />
|Location=Santa Fe Institute<br />
|Attendee list=JacopoGrilli;CaterinaGratton;DietmarPlenz;SusanFitzpatrick;RobertoCabeza;JackGallant;RussPoldrack;PaulGarcia;RandyMcIntosh;ViktorJirsa;RichardFrackowiak;NikolausKriegeskorte;SidneyRedner;NihatAy;Ehren Newman;GuyMiller;Tyler Marghetis;ArtemyKolchinsky<br />
|Post-meeting summary=Coming soon.<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=A_Stab_at_Time&diff=5521A Stab at Time2020-04-24T22:16:58Z<p>AmyPChen: </p>
<hr />
<div>{{Meeting<br />
|Type of meeting=Others<br />
|Start date/time=September 16, 2019<br />
|End date/time=September 17, 2019<br />
|Meeting video=https://www.youtube.com/watch?v=6I0g41R_gOw&list=PLZlVBTf7N6GoAPu-80tFHGLD39e3uidj3&index=8<br />
|Organizers=KaroleArmitage;JohnHarte<br />
|Meeting summary=The public is often intimidated by the complexity of science, seeing it as cold and unfeeling. And yet, without a basic understanding of science, one is ill equipped to make meaningful decisions on a myriad of issues that impact our lives in critical ways. At this meeting we plan to come up with a point of view, scientifically and aesthetically, for a dance production on the subject of time, in connection with the SFI research theme on Complex Time: Adaptation, Aging, Arrow of Time. The meeting will serve as a brainstorming session, with the choreographer, composer, dancer, and scientists talking extensively about time, music, design and the characteristics of the performance. The goal is for everyone involved to understand the nature of how time is to be experienced by the audience, so that everyone’s individual contributions adhere to the same fundamental understanding.<br />
|Attendee list=GregorySpears;JockSoto<br />
|Post-meeting summary=Coming soon.<br />
}}<br />
[[Category:Agenda meetings|Stab]]</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=What_is_Sleep%3F&diff=5520What is Sleep?2020-04-24T22:14:59Z<p>AmyPChen: </p>
<hr />
<div>{{Meeting<br />
|Type of meeting=Application Area<br />
|Application area=Sleep<br />
|Start date/time=November 18, 2019<br />
|End date/time=November 20, 2019<br />
|Meeting video=https://www.youtube.com/watch?v=3HlWAogZnvI&list=PLZlVBTf7N6GoAPu-80tFHGLD39e3uidj3&index=9<br />
|Organizers=VanSavage;AlexHerman<br />
|Meeting summary=Sleep is ubiquitous and a necessity for virtually any organism with some form of a brain. Yet the dominant causes and functions of sleep remain a mystery within species, across species, across development, and across daily cycles of night and day. Moreover, understanding how these different time scales and potentially different functions of sleep at each time scale are able to interact and integrate is a major challenge. For instance, sleep times decrease with body size across species and also decrease with body size as organisms grow from birth to adult. However, the rate of change with body size is very different across phylogeny than it is across ontogeny. In addition, it is intriguing to consider how biological and physical clocks can be coupled together. Biological clocks change with species and age, but the physical clocks of the sun, moon, and seasons are experienced to be the same by all organisms. This is further complicated by the fact that some species live only a few days while others can live for 200 years. Consequently, this working group will focus on the causes, time scales, and consequences of sleep for the following aspects:<br />
<br />
• Changes in sleep time across species (evolution and physiology)<br />
<br />
• Changes in sleep time as we grow (early and late development)<br />
<br />
• Changes in sleep time as we age during adulthood<br />
<br />
• Changes in when we sleep (circadian, consolidated, etc.)<br />
<br />
• Changes in sleep time within a single sleep cycle (REM and non-REM)<br />
|Attendee list=GeoffreyWest;MarishkaBrown;CeciliaDinizBehn;SaraAton;ElizabethKlerman;JeromeSiegel;GinaPoe;SusanSara;RobertStickgold;VictoriaBooth;KimberleyWhitehead;Junyu Cao<br />
|Post-meeting summary=Coming soon!<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=What_is_Sleep%3F&diff=5519What is Sleep?2020-04-24T20:50:24Z<p>AmyPChen: </p>
<hr />
<div>{{Meeting<br />
|Type of meeting=Application Area<br />
|Application area=Sleep<br />
|Start date/time=November 18, 2019<br />
|End date/time=November 20, 2019<br />
|Meeting video=https://www.youtube.com/watch?v=6I0g41R_gOw&list=PLZlVBTf7N6GoAPu-80tFHGLD39e3uidj3&index=8<br />
|Organizers=VanSavage;AlexHerman<br />
|Meeting summary=Sleep is ubiquitous and a necessity for virtually any organism with some form of a brain. Yet the dominant causes and functions of sleep remain a mystery within species, across species, across development, and across daily cycles of night and day. Moreover, understanding how these different time scales and potentially different functions of sleep at each time scale are able to interact and integrate is a major challenge. For instance, sleep times decrease with body size across species and also decrease with body size as organisms grow from birth to adult. However, the rate of change with body size is very different across phylogeny than it is across ontogeny. In addition, it is intriguing to consider how biological and physical clocks can be coupled together. Biological clocks change with species and age, but the physical clocks of the sun, moon, and seasons are experienced to be the same by all organisms. This is further complicated by the fact that some species live only a few days while others can live for 200 years. Consequently, this working group will focus on the causes, time scales, and consequences of sleep for the following aspects:<br />
<br />
• Changes in sleep time across species (evolution and physiology)<br />
<br />
• Changes in sleep time as we grow (early and late development)<br />
<br />
• Changes in sleep time as we age during adulthood<br />
<br />
• Changes in when we sleep (circadian, consolidated, etc.)<br />
<br />
• Changes in sleep time within a single sleep cycle (REM and non-REM)<br />
|Attendee list=GeoffreyWest;MarishkaBrown;CeciliaDinizBehn;SaraAton;ElizabethKlerman;JeromeSiegel;GinaPoe;SusanSara;RobertStickgold;VictoriaBooth;KimberleyWhitehead;Junyu Cao<br />
|Post-meeting summary=Coming soon!<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Aging_and_Adaptation_in_Infectious_Diseases_III/Session_I:_Immune_System:_Innate/Adaptive_collaboration&diff=5513Aging and Adaptation in Infectious Diseases III/Session I: Immune System: Innate/Adaptive collaboration2020-04-10T19:54:08Z<p>AmyPChen: </p>
<hr />
<div>{{Agenda item<br />
|Start time=January 14, 2020 09:30:00 AM<br />
|End time=January 14, 2020 12:00:00 PM<br />
|Is presentation=No<br />
|Description='''(20 minute presentations+10 minute discussion; general discussion at the end)''' <br />
<br />
'''Moderator: Mercedes Pascual'''<br />
|Agenda sub-items={{Agenda sub-item<br />
|Presenter=MicaelaMartinez<br />
|Description=Fast & Slow Immunology: Can we frame predictable temporal trajectories in immunity? Review and Perspectives A<br />
}}{{Agenda sub-item<br />
|Presenter=AndreaLGraham<br />
|Description=Review and Perspectives B<br />
}}{{Agenda sub-item<br />
|Presenter=EricJones;JeanCarlson<br />
|Description=Immunosenosence in Coupled Models of Innate/Adaptive Immune Responses A<br />
|Pre-meeting notes=While participating in the Aging and Adaptation in Infectious Diseases working group, we refined our mathematical model of the immune system based on expert feedback from other participants. In particular, we discussed parameterizing our model based on existing experimental data of how human memory and naive cell populations change with age. We received several recommendations for relevant studies that we were unaware of before the meeting. Additionally, we discussed how our understanding of the immune model could be improved by a thorough bifurcation analysis, and in particular how this analysis might indicate sensitive parameters that can help quantify immune risk. We discussed how our model could be modified in future work to be applicable to influenza: in particular, influenza rapidly mutates and so considerations of cross-reactive antibodies need to be considered (which our model does not currently include). Future work could also focus on the coevolving feedbacks between our immune model and pathogen strains, and in particular how the evolutionary pressures of an adaptive immune response drive can drive the evolution of diversity of pathogens. Participants expressed interest in studying how chronic infections affect immune outcomes, focusing in particular on cytomegalovirus and its debilitating effect on a host's immune response. Lastly, we have entered into exciting new discussions with Chris Kempes and Andy Dobson regarding how immune system responses scale with host size, which might reveal how immune behaviors are conserved across species' size and age.<br />
}}{{Agenda sub-item<br />
|Presenter=ShenshenWang;JimingSheng<br />
|Description=Immunosenosence in Coupled Models of Innate/Adaptive Immune Responses B<br />
}}<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life/Discussion&diff=5489Aging in Single-celled Organisms: from Bacteria to the Whole Tree of Life/Discussion2020-02-12T19:19:26Z<p>AmyPChen: </p>
<hr />
<div>{{Agenda item<br />
|Start time=February 12, 2020 09:00:00 AM<br />
|End time=February 12, 2020 12:00:00 PM<br />
|Is presentation=No<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=File:Santa_fe2020_aging_(1).pdf&diff=5481File:Santa fe2020 aging (1).pdf2020-02-12T05:01:58Z<p>AmyPChen: User created page with UploadWizard</p>
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|date=<br />
|source={{own}}<br />
|author=[[User:AmyPChen|AmyPChen]]<br />
|permission=<br />
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<br />
[[Category:Uploaded via Campaign:Presentation file]]</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life/Discussion&diff=5468Aging in Single-celled Organisms: from Bacteria to the Whole Tree of Life/Discussion2020-02-11T23:12:18Z<p>AmyPChen: Created page with "{{Agenda item |Start time=February 11, 2020 02:00:00 PM |End time=February 11, 2020 05:00:00 PM |Is presentation=No }}"</p>
<hr />
<div>{{Agenda item<br />
|Start time=February 11, 2020 02:00:00 PM<br />
|End time=February 11, 2020 05:00:00 PM<br />
|Is presentation=No<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life/A_time_to_sleep_and_a_time_to_die&diff=5467Aging in Single-celled Organisms: from Bacteria to the Whole Tree of Life/A time to sleep and a time to die2020-02-11T20:36:50Z<p>AmyPChen: Created page with "{{Agenda item |Start time=February 11, 2020 01:30:00 PM |End time=February 11, 2020 02:00:00 |Is presentation=No |Presenter=GeoffreyWest }}"</p>
<hr />
<div>{{Agenda item<br />
|Start time=February 11, 2020 01:30:00 PM<br />
|End time=February 11, 2020 02:00:00 <br />
|Is presentation=No<br />
|Presenter=GeoffreyWest<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life/Time_perception_and_the_rate_of_cellular_aging_outside_the_human_body:_an_energetic_perspective&diff=5466Aging in Single-celled Organisms: from Bacteria to the Whole Tree of Life/Time perception and the rate of cellular aging outside the human body: an energetic perspective2020-02-11T18:39:37Z<p>AmyPChen: Created page with "{{Agenda item |Start time=February 11, 2020 11:30:00 AM |End time=February 11, 2020 12:00:00 PM |Is presentation=No |Presenter=MartinPicard }}"</p>
<hr />
<div>{{Agenda item<br />
|Start time=February 11, 2020 11:30:00 AM<br />
|End time=February 11, 2020 12:00:00 PM<br />
|Is presentation=No<br />
|Presenter=MartinPicard<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life/Systematic_Physiology_and_Aging_Across_Diverse_Organisms&diff=5465Aging in Single-celled Organisms: from Bacteria to the Whole Tree of Life/Systematic Physiology and Aging Across Diverse Organisms2020-02-11T17:54:08Z<p>AmyPChen: Created page with "{{Agenda item |Start time=February 11, 2020 10:15:00 AM |End time=February 11, 2020 10:45:00 AM |Is presentation=No |Presenter=ChrisKempes }}"</p>
<hr />
<div>{{Agenda item<br />
|Start time=February 11, 2020 10:15:00 AM<br />
|End time=February 11, 2020 10:45:00 AM<br />
|Is presentation=No<br />
|Presenter=ChrisKempes<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life&diff=5464Aging in Single-celled Organisms: from Bacteria to the Whole Tree of Life2020-02-11T16:51:09Z<p>AmyPChen: </p>
<hr />
<div>{{Meeting<br />
|Type of meeting=Application Area<br />
|Application area=Cellular Aging<br />
|Start date/time=February 10, 2020<br />
|End date/time=February 12, 2020<br />
|Organizers=JacopoGrilli;ChrisKempes;MatteoOsella;SrividyaIyer-Biswas<br />
|Meeting summary=This working group will bring together experimentalists and theoreticians to better understand the processes and implications of how single-celled organisms age. General principles will be drawn from high-throughput growth and division data of aging single-cells. Energetics by which they store and process information will be connected with those in larger, multicellular organisms. Some key questions this working group will consider include how the aging clock in a single-celled organism is coupled to that of a more complex organism in which it resides (and vise versa), how aging changes with growth and division, how cells with different age process information differently from the environment, and how aging differ across the tree of life. <br />
|Attendee list=MartinPicard;UliSteiner;SabrinaSpencer;LinChao;VanSavage;Bree Aldridge;Owen Jones;GeoffreyWest<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life&diff=5463Aging in Single-celled Organisms: from Bacteria to the Whole Tree of Life2020-02-11T16:50:32Z<p>AmyPChen: </p>
<hr />
<div>{{Meeting<br />
|Type of meeting=Application Area<br />
|Application area=Cellular Aging<br />
|Start date/time=February 10, 2020<br />
|End date/time=February 12, 2020<br />
|Organizers=JacopoGrilli;ChrisKempes;MatteoOsella;SrividyaIyer-Biswas<br />
|Meeting summary=This working group will bring together experimentalists and theoreticians to better understand the processes and implications of how single-celled organisms age. General principles will be drawn from high-throughput growth and division data of aging single-cells. Energetics by which they store and process information will be connected with those in larger, multicellular organisms. Some key questions this working group will consider include how the aging clock in a single-celled organism is coupled to that of a more complex organism in which it resides (and vise versa), how aging changes with growth and division, how cells with different age process information differently from the environment, and how aging differ across the tree of life. <br />
|Attendee list=MartinPicard;UliSteiner;SabrinaSpencer;LinChao;VanSavage;SidneyRedner;Bree Aldridge;Owen Jones;GeoffreyWest<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life/The_long_and_the_short_of_it:_mycobacterial_aging,_asymmetry,_and_stress_tolerance&diff=5462Aging in Single-celled Organisms: from Bacteria to the Whole Tree of Life/The long and the short of it: mycobacterial aging, asymmetry, and stress tolerance2020-02-11T16:26:54Z<p>AmyPChen: Created page with "{{Agenda item |Start time=February 11, 2020 09:15:00 AM |End time=February 11, 2020 09:45:00 AM |Is presentation=No |Presenter=Bree Aldridge }}"</p>
<hr />
<div>{{Agenda item<br />
|Start time=February 11, 2020 09:15:00 AM<br />
|End time=February 11, 2020 09:45:00 AM<br />
|Is presentation=No<br />
|Presenter=Bree Aldridge<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life/Toward_a_Molecular_Understanding_of_Quiescence_versus_Senescence&diff=5460Aging in Single-celled Organisms: from Bacteria to the Whole Tree of Life/Toward a Molecular Understanding of Quiescence versus Senescence2020-02-10T22:55:30Z<p>AmyPChen: Created page with "{{Agenda item |Start time=February 10, 2020 03:45:00 PM |End time=February 10, 2020 04:15:00 PM |Is presentation=No |Presenter=SabrinaSpencer |Pre-meeting notes=Cellular aging..."</p>
<hr />
<div>{{Agenda item<br />
|Start time=February 10, 2020 03:45:00 PM<br />
|End time=February 10, 2020 04:15:00 PM<br />
|Is presentation=No<br />
|Presenter=SabrinaSpencer<br />
|Pre-meeting notes=Cellular aging is often used synonymously with cellular senescence, a state of permanent cell-cycle exit associated with DNA damage and cytokine secretion. However, senescence is easily confused with quiescence, in large part due to lack of reliable markers. We have found that the gold-standard senescence marker, senescence-associated beta-galactosidase activity, is unreliable in that it can stain strongly positive in cells that are actively dividing. We have also found that establishing a homogeneous population of senescent cells is quite difficult since many cells continue to cycle and out-proliferate senescent cells, despite the use of standard senescence-inducing treatments. Thus, the senescence field has a chicken/egg problem in that one cannot study senescence if no reliable markers exist to identify senescent cells, and one cannot develop a senescence marker without a truly senescent sample in hand. We are therefore developing a functional readout to identify cells that have not cycled in ''n'' days, where ''n'' is triggered and defined by the researcher and can be several months long. In this way, we can isolate a homogeneous senescent population that can be profiled and compared to quiescent cells to develop better markers for quiescence vs. senescence and to better study cellular aging.<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life/All_creatures_fast_and_slow:_senescence_and_longevity_across_the_tree_of_life&diff=5459Aging in Single-celled Organisms: from Bacteria to the Whole Tree of Life/All creatures fast and slow: senescence and longevity across the tree of life2020-02-10T21:50:08Z<p>AmyPChen: Created page with "{{Agenda item |Start time=February 10, 2020 02:30:00 PM |End time=February 10, 2020 03:00:00 |Is presentation=No |Presenter=Owen Jones }}"</p>
<hr />
<div>{{Agenda item<br />
|Start time=February 10, 2020 02:30:00 PM<br />
|End time=February 10, 2020 03:00:00 <br />
|Is presentation=No<br />
|Presenter=Owen Jones<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life/About_time:_Precision_measurements_and_emergent_simplicities_in_an_individual_bacterial_cell%27s_stochastic_aging_dynamics.&diff=5458Aging in Single-celled Organisms: from Bacteria to the Whole Tree of Life/About time: Precision measurements and emergent simplicities in an individual bacterial cell's stochastic aging dynamics.2020-02-10T20:46:14Z<p>AmyPChen: Created page with "{{Agenda item |Start time=February 10, 2020 01:30:00 PM |End time=February 10, 2020 02:00:00 PM |Is presentation=No |Presenter=SrividyaIyer-Biswas }}"</p>
<hr />
<div>{{Agenda item<br />
|Start time=February 10, 2020 01:30:00 PM<br />
|End time=February 10, 2020 02:00:00 PM<br />
|Is presentation=No<br />
|Presenter=SrividyaIyer-Biswas<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life/Stochastic_processes_shape_senescence,_beyond_genes,_and_environment&diff=5457Aging in Single-celled Organisms: from Bacteria to the Whole Tree of Life/Stochastic processes shape senescence, beyond genes, and environment2020-02-10T19:02:05Z<p>AmyPChen: </p>
<hr />
<div>{{Agenda item<br />
|Start time=February 10, 2020 11:45:00 AM<br />
|End time=February 10, 2020 12:15:00 PM<br />
|Is presentation=No<br />
|Presenter=UliSteiner<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life/Stochastic_processes_shape_senescence,_beyond_genes,_and_environment&diff=5456Aging in Single-celled Organisms: from Bacteria to the Whole Tree of Life/Stochastic processes shape senescence, beyond genes, and environment2020-02-10T19:01:39Z<p>AmyPChen: Created page with "{{Agenda item |Start time=February 10, 2020 11:45:00 AM |End time=February 10, 2020 12:15:00 PM |Is presentation=No }}"</p>
<hr />
<div>{{Agenda item<br />
|Start time=February 10, 2020 11:45:00 AM<br />
|End time=February 10, 2020 12:15:00 PM<br />
|Is presentation=No<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life/Stochasticity,_immortality,_and_mortality_in_E._coli&diff=5455Aging in Single-celled Organisms: from Bacteria to the Whole Tree of Life/Stochasticity, immortality, and mortality in E. coli2020-02-10T17:59:55Z<p>AmyPChen: Created page with "{{Agenda item |Start time=February 10, 2020 10:45:00 AM |End time=February 10, 2020 11:15:00 |Is presentation=No |Presenter=LinChao |Pre-meeting notes=Here we show that the b..."</p>
<hr />
<div>{{Agenda item<br />
|Start time=February 10, 2020 10:45:00 AM<br />
|End time=February 10, 2020 11:15:00 <br />
|Is presentation=No<br />
|Presenter=LinChao<br />
|Pre-meeting notes=Here we show that the bacterium Escherichia coli exhibits both lineage mortality and immortality. The outcome depends on a whether a balance is achieved between damage accumulation and the asymmetric allocation of damage from mother to daughters. At low damage rates, both old and new daughters, which are allocated respectively more and less damage, generated immortal lineages that achieved stable growth rate equilibria. At high rates, mortality ensued because while the new daughter lineage persisted, the old daughter lineage stopped dividing. The stoppage was found to result from an increase in the stochasticity of cell growth.<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life/More_questions_than_answers:_relations_between_quantittative_physiology_and_aging_in_E._coli&diff=5454Aging in Single-celled Organisms: from Bacteria to the Whole Tree of Life/More questions than answers: relations between quantittative physiology and aging in E. coli2020-02-10T16:36:59Z<p>AmyPChen: Created page with "{{Agenda item |Start time=February 10, 2020 09:30:00 AM |End time=February 10, 2020 10:00:00 AM |Is presentation=No |Presenter=Matteo Osella }}"</p>
<hr />
<div>{{Agenda item<br />
|Start time=February 10, 2020 09:30:00 AM<br />
|End time=February 10, 2020 10:00:00 AM<br />
|Is presentation=No<br />
|Presenter=Matteo Osella<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life/Overview_of_the_meeting&diff=5453Aging in Single-celled Organisms: from Bacteria to the Whole Tree of Life/Overview of the meeting2020-02-10T15:42:00Z<p>AmyPChen: Created page with "{{Agenda item |Start time=February 10, 2020 09:00:00 AM |End time=February 10, 2020 09:30:00 AM |Is presentation=No |Presenter=JacopoGrilli }}"</p>
<hr />
<div>{{Agenda item<br />
|Start time=February 10, 2020 09:00:00 AM<br />
|End time=February 10, 2020 09:30:00 AM<br />
|Is presentation=No<br />
|Presenter=JacopoGrilli<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life/Day_1_Continental_Breakfast_(outside_SFI_Collins_Conference_Room)&diff=5452Aging in Single-celled Organisms: from Bacteria to the Whole Tree of Life/Day 1 Continental Breakfast (outside SFI Collins Conference Room)2020-02-10T15:40:17Z<p>AmyPChen: Created page with "{{Agenda item |Start time=February 10, 2020 08:30:00 AM |End time=February 10, 2020 09:00:00 AM |Is presentation=No }}"</p>
<hr />
<div>{{Agenda item<br />
|Start time=February 10, 2020 08:30:00 AM<br />
|End time=February 10, 2020 09:00:00 AM<br />
|Is presentation=No<br />
}}</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=MediaWiki:Masspasswordreset_email_body&diff=5442MediaWiki:Masspasswordreset email body2020-02-01T21:23:46Z<p>AmyPChen: </p>
<hr />
<div>Hi $1,<br />
<br />
Thank you for participating in the Santa Fe Institute (SFI) '''"Aging in Single-celled Organisms: from Bacteria to the Whole Tree of Life"''' working group (WG), 2/10/2020 - 2/12/2020, co-organized by Jacopo Grilli (ICTP), Srividya Iyer-Biswas (Purdue Univ.), Chris Kempes (SFI), and Matteo Osella (Univ. Turin). This WG is part of the SFI [https://www.santafe.edu/research/themes/complex-time ''Complex Time: Adaptation, Aging, & the Arrow of Time''] research theme, funded by the [https://www.jsmf.org/ James S. McDonnell Foundation].<br />
<br />
We will be using the SFI Complex Time wiki to capture and share important meeting information during the meeting.<br />
<br />
The '''"ging in Single-celled Organisms WG"''' page is [https://centre.santafe.edu/complextime/Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life here].<br />
<br />
Please use the following log-in details:<br />
<br />
Username: $1<br /><br />
Password (randomly generated; be careful not to copy an extra space before/after): $2<br />
<br />
''You can change your password once you have logged in, by going to the wiki top right corner, blue people icon -> Preferences, scroll down to the "Basic information" box, where it says Password: Change password. If you ever forget your password, you can follow the "forget your password" on the wiki log in page, or ask Amy to reset your password (contact her at amypchen@santafe.edu).''<br />
<br />
- Two ways to contribute <span style="color:#fc3">'''Meeting Reflection'''</span>, <span style="color:#fc3">'''References'''</span>, and <span style="color:#fc3">'''Reference Notes'''</span>: (1) click [https://centre.santafe.edu/complextime/w/index.php?title=Special:Userlogin&returnto=Special%3ARunQuery%2FAttendee+note+query&returntoquery=Attendee+note%5BMeeting%5D%3DAging+in+Single-celled+Organisms%3A+from+Bacteria+to+the+Whole+Tree+of+Life%26_run here] (you will be prompted to log in first) (2) from the [https://centre.santafe.edu/complextime/Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life meeting wiki], click on the box on the left-hand side of the page that says <span style="color:#fff; background:#2a4b8d">'''Add or edit your own meeting material'''</span> (you will be prompted to log in first).<br />
<br />
<span style="color:#fc3">'''Meeting Reflections''' </span> are 1+ paragraphs on any combination of the following: Presentation highlights, open questions that came up, how your perspective changed, impact on your own work, e.g. the discussion on [A] that we are having reminds me of [B] conference/[C] initiative/[D] funding call-for-proposal/[E] research group<br />
<br />
By <span style="color:#fc3">'''References''' </span> we don't only mean your own work related to this WG, but also synergistic work you know of elsewhere, especially those you think of or mentioned to the group during the group discussion. <br />
<br />
By <span style="color:#fc3">'''Reference Notes''' </span> we mean some documentations about the references that you are adding, for example: "Here is [A] database on [B] that I pull data from to do [C] analysis that might be of interest to this group (provide link)", "here is a free tool for calculating [ABC] (provide link)", "this painting/sculpture/forms of artwork is emblematic to our discussion on [X]!", "Schwartz et al. 2017 offers a review on [ABC] migration as relate to climatic factors"<br />
<br />
-<span style="color:#fc3">'''To comment on another participant's meeting reflection''' </span>: go to the [https://centre.santafe.edu/complextime/Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life meeting wiki], scroll down to the '''"Meeting Summary"''' tab, click on '''"Add comment"''' (note that you CAN type math expressions and symbols).<br />
<br />
-To upload your <span style="color:#00af89">'''presentation slides''' </span>: go to the [https://centre.santafe.edu/complextime/Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life meeting page], scroll down to the '''"Agenda"''' tab, locate and click on your talk title hyperlink, click on <span style="color:#fff; background:#36c">'''UPLOAD A PRESENTATION FILE'''</span>. Note that it's possible to encrypt your file (follow the prompts during file upload) if you only want to share it with a selected group of people. Participants in this meeting will automatically be shown the encryption key that allows them to download the file once they are logged in. You can also send the encryption key to anyone you want to have access to the file who did not participate in this meeting. <br />
<br />
Questions? Report bugs, comments & suggestions about the wiki to Amy P. Chen (amypchen@santafe.edu) &/or Ike Hecht (ikehecht@wikiworks.com).</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=MediaWiki:Masspasswordreset_email_body&diff=5441MediaWiki:Masspasswordreset email body2020-02-01T21:18:28Z<p>AmyPChen: </p>
<hr />
<div>Hi $1,<br />
<br />
Thank you for participating in the Santa Fe Institute (SFI) '''"Aging in Single-celled Organisms: from Bacteria to the Whole Tree of Life"''' working group (WG), 2/10/2020 - 2/12/2020, co-organized by Jacopo Grilli (ICTP), Srividya Iyer-Biswas (Purdue Univ.), Chris Kempes (SFI), and Matteo Osella (Univ. Turin). This WG is part of the SFI [https://www.santafe.edu/research/themes/complex-time ''Complex Time: Adaptation, Aging, & the Arrow of Time''] research theme, funded by the [https://www.jsmf.org/ James S. McDonnell Foundation].<br />
<br />
We will be using the SFI Complex Time wiki to capture and share important meeting information during the meeting.<br />
<br />
The '''"Aging and Adaptation in Infectious Diseases III WG"''' page is [https://centre.santafe.edu/complextime/Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life here].<br />
<br />
Please use the following log-in details:<br />
<br />
Username: $1<br /><br />
Password (randomly generated; be careful not to copy an extra space before/after): $2<br />
<br />
''You can change your password once you have logged in, by going to the wiki top right corner, blue people icon -> Preferences, scroll down to the "Basic information" box, where it says Password: Change password. If you ever forget your password, you can follow the "forget your password" on the wiki log in page, or ask Amy to reset your password (contact her at amypchen@santafe.edu).''<br />
<br />
- Two ways to contribute <span style="color:#fc3">'''Meeting Reflection'''</span>, <span style="color:#fc3">'''References'''</span>, and <span style="color:#fc3">'''Reference Notes'''</span>: (1) click [https://centre.santafe.edu/complextime/w/index.php?title=Special:Userlogin&returnto=Special%3ARunQuery%2FAttendee+note+query&returntoquery=Attendee+note%5BMeeting%5D%3DAging+in+Single-celled+Organisms%3A+from+Bacteria+to+the+Whole+Tree+of+Life%26_run here] (you will be prompted to log in first) (2) from the [https://centre.santafe.edu/complextime/Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life meeting wiki], click on the box on the left-hand side of the page that says <span style="color:#fff; background:#2a4b8d">'''Add or edit your own meeting material'''</span> (you will be prompted to log in first).<br />
<br />
<span style="color:#fc3">'''Meeting Reflections''' </span> are 1+ paragraphs on any combination of the following: Presentation highlights, open questions that came up, how your perspective changed, impact on your own work, e.g. the discussion on [A] that we are having reminds me of [B] conference/[C] initiative/[D] funding call-for-proposal/[E] research group<br />
<br />
By <span style="color:#fc3">'''References''' </span> we don't only mean your own work related to this WG, but also synergistic work you know of elsewhere, especially those you think of or mentioned to the group during the group discussion. <br />
<br />
By <span style="color:#fc3">'''Reference Notes''' </span> we mean some documentations about the references that you are adding, for example: "Here is [A] database on [B] that I pull data from to do [C] analysis that might be of interest to this group (provide link)", "here is a free tool for calculating [ABC] (provide link)", "this painting/sculpture/forms of artwork is emblematic to our discussion on [X]!", "Schwartz et al. 2017 offers a review on [ABC] migration as relate to climatic factors"<br />
<br />
-<span style="color:#fc3">'''To comment on another participant's meeting reflection''' </span>: go to the [https://centre.santafe.edu/complextime/Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life meeting wiki], scroll down to the '''"Meeting Summary"''' tab, click on '''"Add comment"''' (note that you CAN type math expressions and symbols).<br />
<br />
-To upload your <span style="color:#00af89">'''presentation slides''' </span>: go to the [https://centre.santafe.edu/complextime/Aging_in_Single-celled_Organisms:_from_Bacteria_to_the_Whole_Tree_of_Life meeting page], scroll down to the '''"Agenda"''' tab, locate and click on your talk title hyperlink, click on <span style="color:#fff; background:#36c">'''UPLOAD A PRESENTATION FILE'''</span>. Note that it's possible to encrypt your file (follow the prompts during file upload) if you only want to share it with a selected group of people. Participants in this meeting will automatically be shown the encryption key that allows them to download the file once they are logged in. You can also send the encryption key to anyone you want to have access to the file who did not participate in this meeting. <br />
<br />
Questions? Report bugs, comments & suggestions about the wiki to Amy P. Chen (amypchen@santafe.edu) &/or Ike Hecht (ikehecht@wikiworks.com).</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=MediaWiki:Masspasswordreset_email_subject&diff=5440MediaWiki:Masspasswordreset email subject2020-02-01T21:13:33Z<p>AmyPChen: </p>
<hr />
<div>SFI Aging in Single-celled Organisms WG (2/10 - 2/12/2020)</div>AmyPChenhttps://centre.santafe.edu/complextime/w/index.php?title=Aging_and_Adaptation_in_Infectious_Diseases_III/Optional_additional_Working_Group_Sessions_(for_those_staying_that_afternoon)&diff=5425Aging and Adaptation in Infectious Diseases III/Optional additional Working Group Sessions (for those staying that afternoon)2020-01-14T04:39:56Z<p>AmyPChen: Created page with "{{Agenda item |Start time=January 17, 2020 01:30:00 PM |End time=January 17, 2020 05:00:00 PM |Is presentation=No }}"</p>
<hr />
<div>{{Agenda item<br />
|Start time=January 17, 2020 01:30:00 PM<br />
|End time=January 17, 2020 05:00:00 PM<br />
|Is presentation=No<br />
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