4:00

Energy Allostasis: Uncovering The Hidden Link Between Metabolic And Mental Health
Camilla L. Nord
MRC Cognition and Brain Sciences Unit, University of Cambridge, Cambridge, United Kingdom

To survive, our brain must accurately predict internal states, enabling flexible, prospective regulation of the body’s physiology, or ‘allostasis’: eating before starvation, drinking before dehydration. Wide-ranging studies report a disruption in allostatic mechanisms in mental health disorders, potentially driving clinical features such as appetite dysregulation in major depression as well as known epidemiological comorbidity between depression and poor metabolic health. I will discuss a series of cognitive-computational neuroscience experiments investigating the overlap between mental and metabolic health, including finding that depression and diabetes are both associated with disruptions in effort-based decision-making, and that mental and metabolic health is associated with changes in reinforcement learning. I will situate these cognitive mechanisms in a broader model of energy allostasis as a link between disruptions to metabolism and mental health.

10:00

Shaping The Next Generation: The Impact Of Barbara Rolls&Rsquo; Mentorship On The Field Of Ingestive Behavior
Paige Cunningham
Cornell University, Ithaca, NY, United States

Over a highly impactful career spanning decades, Barbara Rolls has left a giant footprint and proved to be a true luminary in the field of ingestive behavior. Beyond her own work, through her dedication to mentorship Barbara has and continues to shape the next generation of scientists. As her last graduate student, Barbara’s mentorship echoes throughout my work and career. Our mechanistic investigation of sensory-specific satiety and hedonic determinants of meal intake contributed to our discovery of switching (alternations between meal components) as a behavior that is significantly associated with food intake in adults and children. Our investigation of the combined effects of variety and portion size highlights the need to consider how properties of food known to influence consumption can work together to drive greater energy intake than either property alone. And together, we developed The Satiation Framework, which moves beyond a focus on physiological fullness to consider satiation as a series of dynamic processes that drive meal termination. This framework informs my multidisciplinary approach to understanding determinants of energy intake at meals. Overall, Barbara’s mentorship has influenced not only the research questions that I hope to pursue over the course of my career, but also the way I approach science as a whole – with rigor, with intentionality, and with consideration of real-world implications and how our work can meaningfully benefit human health. So, while I am Barbara’s last graduate student, I see this not as an end of an era but as a start of the next generation, still very much shaped by the remarkable mentorship of Barbara Rolls.

10:30

From (Controlled) Plate To Paradigm: Honoring A Pioneer Of Portion Size And Energy Density Research
Jennifer O. Fisher
Temple University, Philadelphia, PA, United States

This talk will reflect on the scientific contributions and legacy of Barbara J. Rolls, whose research established portion size and energy density as fundamental determinants of food and energy intake in both children and adults. Drawing on my experiences as a graduate student at Penn State, I will highlight the culture of inquiry and methodological rigor that Barbara fostered, which has shaped my approach to science, as well as that of many others under her tutelage. I will describe how her research on portion size and energy density has shaped key concepts about the regulation of intake and stimulated subsequent work in pediatric populations, including my own. Finally, I will discuss how this evidence has been translated into policy-relevant implications, underscoring the substantial public health impact of her contributions. Central to Barbara’s legacy is a commitment to conceptual clarity and rigorous methodology, reflected in the elegant design of her controlled feeding studies and her persistent effort to understand eating behavior from multiple perspectives. This influence endures not only in the body of evidence she produced, but also in the many investigators whose approaches to studying eating behavior remain grounded in her work.

11:00

High Volume, High Impact: The Barbara Rolls Effect
Alexandria B Hast
The Campbell's Company, Camden, NJ, United States

Dr. Barbara Rolls has dedicated her career to understanding the fundamental drivers of food intake, producing a body of work on energy density, portion size, and dietary composition that is among the most cited and applied in nutritional science. That scientific legacy extends well beyond publications; it has shaped the careers of an entire generation of researchers now working across academia, government, and industry. Graduate training in the Rolls laboratory is defined by intellectual rigor and careful experimental design. These core competencies translate directly into high-impact careers, including in the food industry, where evidence-based thinking, regulatory fluency, and the ability to connect nutrition science to consumer behavior are increasingly in demand. Effective mentorship develops scientists who can operate at the boundary between discovery and application; and, Barbara Rolls has exemplified this role for decades.

11:30

Translating Science To Improve Health: Using Research To Support Evidence-Based Public Health Nutrition Decision-Making
Julie Obbagy
USDA, Medfield, MA, United States

Barbara Rolls’ mentorship directly impacted my decision to pursue a career in the Federal government translating science to improve health. My career involves developing, advancing, and applying methods to conduct systematic reviews and other evidence synthesis projects that examine the complex interplay between diet and health. The values required of gold standard evidence synthesis processes - identification of high-priority research questions, scientific rigor and transparency, management of biases and conflicts of interest, diversity of expertise and collaboration, and effective science communication - are all values that were central to my training experience with Barbara Rolls. Systematic reviews that are high-quality and trustworthy are critical for end users who use their findings to make evidence-based decisions that have real-world public health impact. A recent systematic review that examined the relationship between portion size and energy intake will be described to demonstrate how research is used to support evidence-based public health nutrition decision-making - and to illustrate the strength of Barbara Rolls’ research program.

3:00

Fgf21 Signals Through Hindbrain Neurons To Alter Food Intake And Energy Expenditure During Dietary Protein Restriction
Redin A. Spann, Sora Q. Kim, Md Shahjalal Khan, Diana A. Albarado, Sun O. Fernandez-Kim, Hans-Rudolf Berthoud, David H. McDougal, Heike Muenzberg, Yanlin He, Sangho Yu, Christopher D. Morrison
Pennington Biomedical Research Center, Baton Rouge, LA, United States

Animals detect and respond to variations in nutrient availability, including reductions in dietary protein availability. Our work has established that the liver-derived metabolic hormone FGF21 is critical for adaptive responses to dietary protein restriction, and that it acts directly within the brain to mediate these effects. However, the precise neural circuit mediating these effects remains undefined. Here, we demonstrate that a discrete population of glutamatergic, Klb-expressing neurons in the nucleus of the solitary tract (NTS) mediates FGF21 action during protein restriction. Using a Klb-Flp mouse line combined with intersectional genetics, we show that NTS-KLB neurons are directly activated by FGF21. Systematic evaluation of previously implicated regions (SCN, PVN, VMH) reveals these areas are not required for FGF21-mediated responses to protein restriction. In contrast, selective ablation of NTS-KLB neurons prevents metabolic adaptations to protein restriction, including changes in food intake, food choice, and energy expenditure, while their chemogenetic activation is sufficient to drive these responses. These findings establish that NTS-KLB neurons directly respond to FGF21 and coordinate adaptive changes during protein restriction, identifying the neural circuit linking dietary protein sensing to metabolic adaptation.

3:30

To Be Announced
ANDREW WANG

4:00

Acute Prefrontal Cortex Response (By Functional Near Infra-Red Spectroscopy, Fnirs) To Ingestion Of Protein And Protein Preloads In Humans: Effects On Satiation Efficacy Rate And Subsequent Acute Intake Of Ultra-Processed Food.
Jennifer A Nasser
Drexel University, Philadelphia, PA, United States

Protein is accepted as the most satiating of all macronutrients as well as the macronutrient promoting the greatest satiety interval. Of current relevance to the US diet is the low level of protein per serving (~2 grams or less/100 kcal serving) contained in most ultra-processed foods (UPF), which make up close to 70% of daily caloric intake. This sparked my interest in the potential for proteins to promote satiation if protein ingestion occurred in close proximity to ingestion of UPF. Additionally, I have had an interest in examining the acute effect of protein ingestion on the prefrontal cortex (PFC) response in adult humans under satiating conditions to probe for potential mechanisms of satiation promotion. For this symposium I will present data from studies of protein ingestion as well as protein preload ingestion effects on subsequent acute intake of UPF with respect to regional activation in the PFC (assess by functional near infra-red spectroscopy, fNIRS) and describe a complementary study of protein ingestion effects in rodents assessed under a common protocol used in our human studies as a means of demonstrating causative mechanisms of satiation promotion. The main working hypothesis that underscores all of the protein-based studies is that acute food intake is less when dorsolateral PFC activation prior to, or during the eating episode is greater than dorsomedial PFC activation. Data accumulated in the human studies and complementary animal study is supportive of this hypothesis.

10:00

Monoamine Release Dynamics In The Human Amygdala Dissociate Components Of Food Reward
Matt Howe^1,2, Seth Batten¹, Leonardo Barbosa¹, Monica Ahrens³, Terry Lohrenz¹, Jason White¹, Robert Bina⁴, Mark Witcher^1,5, Read Montague^1,6, Alexandra DiFeliceantonio^1,7
¹Fralin Biomedical Research Institute at Virginia Tech, Roanoke, VA, United States, ²School of Neuroscience, Virgi, Blacksburg, VA, United States, ³University of Kentucky Medical Center, Kansas City, KS, United States, ⁴Department of Neurosurgery, Banner University Medical Center , Phoenix, AZ, United States, ⁵Department of Neurosurgery, Virginia Tech Carillion School of Medicine, Roanoke, VA, United States, ⁶Department of Physics, Virginia Tech, Blacksburg, VA, United States, ⁷Department of Human Nutrition, Foods, and Exercise, Virginia Tech, Blacksburg, VA, United States

The decision-making process that drives food choice can potently modify overall health and disease risk. Studies, largely conducted in rodents, have underscored the importance of reward-related signals in the brain for guiding food choice. These signals can override homeostatic ones, and likely contribute to the ability of energy dense, highly palatable foods to drive poor health outcomes in humans. While many brain circuits have been implicated in the control of such reward-based eating, there is a growing consensus that it is steered by monoamine (dopamine, serotonin, and norepinephrine) release in brain areas like the amygdala. However, many of the key findings that support these ideas have yet to be translated to humans, due in large part to the lack of technologies that enable insights into the temporal dynamics of monoamine release in the human brain that are comparable to those provided by tools optimized for rodents. Recently, our group has been engaged in an effort to bridge this translational gap through the development of an approach that affords sub-second, concurrent detection of all monoamines in the brain of conscious humans. Here, we present results from on-going studies using this approach to study how monoamine neurotransmitter release in the human amygdala is modulated by food-predictive cues (n=10), as well as the valence of primary food rewards (n=8). Our data support a model whereby dopamine and serotonin signal food valence and cue-reward associations through unique patterns of opponent release. Collectively, these findings represent a first-of their kind test of the translatability of key findings from animal models and identify signatures of neurotransmitter release that may ultimately underwrite both adaptive and maladaptive food choices.

10:30

Control Of Ingestion By The Caudal Brainstem
Zachary Knight
University of California, San Francisco, San Francisco, CA, United States

The passage of food through the alimentary canal generates a series of feedback signals that are sensed by the brain and used to control feeding behavior. Many of these signals converge on the caudal brainstem, which contains the key neural circuits that drive meal termination. I will describe our work investigating the dynamics and function of these circuits during ingestion. A central theme is that these circuits control behavior by integrating layers of feedback signals from the mouth and gut. These feedback signals influence behavior both in real-time during ingestion and over longer timescales through learning.

11:00

To Be Determined
Read Montague

1:00

To Be Gip Or Not To Be Gip, That Is The Question
Randy Seeley
University of Michigan

The advent of polyagonists has opened up tremendous new avenues for the pharmacological treatment of obesity. Numerous different combinations are being actively investigated. The gut hormone GIP and its associated receptor are active targets for polyagonists such as tirzepatide and retatrutide that demonstrate superior weight loss to GLP-1R agonists alone. These clear successes belie a dilemma. Reduced GIP receptor activity is associated with resistance to weight gain in mice and relative leanness in humans. Such genetic analyses support the notion that antagonizing the GIP receptor might be an appropriate strategy for weight loss medications. Maritide is a polyclonal antibody that serves as a GIP antagonist conjugated with two GLP-1 agonist peptides. In both pre-clinical and clinical data, maritide also leads to significant weight loss. How can we understand drugs that have the opposite effect on the GIP receptor, both being effective therapeutic strategies? This presentation will review a wide range of preclinical data to explore the underlying neural circuits for the actions of these drugs and explore the potential hypotheses that might resolve the dilemma presented by GIP.

1:00

Understanding Pomc Neurons Heterogeneity In Energy Balance And Beyond
Daniela Cota
INSERM, Neurocentre Magendie, U1215, University of Bordeaux, Bordeaux, France

Hypothalamic pro-opiomelanocortin (POMC) neurons are critical regulators of energy balance. By integrating adiposity and nutrient signals, they classically act to restrain food intake and promote energy expenditure via melanocortin signaling. Genetic disruption of POMC in mice and humans produces hyperphagia and severe, early-onset obesity, underscoring that intact POMC neuron function is indispensable for defending against positive energy balance and obesity pathogenesis. Nevertheless, recent evidence demonstrates that POMC neurons are molecularly and functionally heterogeneous, can stimulate feeding under specific conditions, and become active before food consumption, therefore challenging the traditional view of their satietogenic function. Here I will present published and unpublished data we have generated illustrating the complex roles of hypothalamic POMC neurons in energy balance and beyond.

3:00

Dietary Substitute Sugars&Rsquo; Osmotic Signaling Engages An Ileal Brake To Control Gut Motility And Feeding Via Glp-1�
Arthur Beyder
Enteric Neuroscience Program (ENSP), Division of Gastroenterology and Hepatology, Departments of Medicine and Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN, United States

Modern diets are replete with poorly absorbed sugar substitutes like sugar alcohols (e.g., xylitol) that impose unusually high luminal osmolar loads, yet how the gut senses these non-nutritive osmoles to regulate ingestion is unclear. Here, we show that luminal hyperosmolarity triggers an ileal brake–like response that slows proximal gut transit and suppresses feeding via gut hormone release. In mice, acute gavage of xylitol (vs. iso-osmotic control) caused luminal contents to accumulate in the small intestine while less reached the cecum within ~45 min, indicating region-specific slowing of ileal transit. This occurred alongside a local spike in ileal luminal osmolality (while stomach and colonic contents remained near isotonic), a ~2-fold surge in plasma GLP-1, increased gastric volume (gastric accommodation), and ~60% reduction in short-term food intake, which are all hallmarks of an ileal brake response. We focused on ileal sensing mechanisms and GLP-1–secreting enteroendocrine cells (EECs), which are known coordinators of the ileal brake, as candidate osmosensors. Mechanistic studies showed that hyperosmolar conditions directly excite EECs: patch-clamp recordings from a human L-cell model (QGP-1) revealed a dramatic ~40 mV depolarization and evoked action potentials under hyperosmotic (400 mOsm/kg) vs. iso-osmotic conditions. Similarly, ileal, but not colonic, primary EECs exhibited robust Ca�⁺ influx to hyperosmolar stimuli ex vivo, and hyperosmotic exposure of ileal organoids triggered a 2–3� increase in GLP-1 secretion. These findings identify an ileal epithelial osmosensory pathway that couples luminal hyperosmotic stimuli to L-cell hormone release and gut-brain-gut feedback. By engaging this pathway, non-nutritive osmoles can powerfully modulate GI motility and satiety signals, revealing a mechanistic link between acute exposure to dietary osmolarity and ingestive behavior. Together, these findings reveal dietary osmolarity as a powerful, previously underappreciated signal through which the gut translates modern food composition into hormonal control of motility, satiety, and ingestive behavior.�

3:30

The Role Of Gastrointestinal Mechanosensation In Regulating
Britya Ghosh¹, Catherine Calhoun², Kara Marshall^1,3,4
¹Department of Neuroscience, Baylor College of Medicine, Houston, TX, ²Rice University, Houston, TX, ³Department of Neuroscience, Howard Hughes Medical Institute, ⁴Jan and Duncan Neurological Research Institute at Texas Children�s Hospital, Houston, TX

The stomach distends to accommodate food, and the gastrointestinal (GI) tract is in constant motion as the ingested food is propelled forward. Mechanical cues from the gastrointestinal (GI) tract play an essential role in informing the brain of feeding states and regulating energy homeostasis, yet it is not well studied. While chemosensory signals, such as leptin and ghrelin, are well known, how mechanical signals induced by stomach distention contribute to energy homeostasis remains poorly defined. PIEZO1 and PIEZO2 are mechanosensory ion channels which are expressed in different organs throughout the body, including neurons that innervate the gastrointestinal tract. They open in response to mechanical force and relay mechanosensory signals via the peripheral nervous system, and are excellent candidates for the sensors that detect mechanical signals to control food intake. Previous work identified oxytocin-receptor�expressing (Oxtr+) sensory neurons as key mechanosensors that detect stretch and relay the sense of satiety to the brain. We are using Oxtr-Cre animals in combination with other genetic tools to delete PIEZO ion channels from subsets of sensory neurons and delineate how these ion channels function to modulate food intake. We found that loss of Piezo2 in Oxtr+ neurons, as well as more broadly in the sensory nervous system, altered feeding patterns despite normal body composition. We further examined hypothalamic neurons in the arcuate to determine how central feeding circuitry was engaged in the absence of mechanosensory signaling. By revealing a mechanosensory pathways parallel to established chemosensory systems, these findings open avenues for developing next-generation anti-obesity therapeutics that tap into mechanical signaling besides targeting the chemical pathways which, despite their efficacy, carry significant gastrointestinal and systemic side effects.

4:00

Pharyngeal Mechanosensation Drives Rapid Thirst Satiation
Sung-Yon Kim
Seoul National University, Seoul, South Korea

Drinking rapidly quenches thirst within seconds, a critical pre-systemic feedback that occurs well before absorbed water restores systemic balance. However, the sensory origin and neural mechanism underlying this rapid thirst satiation have remained elusive. Here, we dissociated tightly coupled processes of drinking to reveal that pharyngeal mechanosensation during the swallowing reflexes is the source of this rapid thirst satiation. This signal primarily depends on PIEZO2 in the nodose-jugular-petrosal ganglia and ascends through a pathway linking the nucleus of the solitary tract, parabrachial nucleus, and median preoptic area, ultimately inhibiting subfornical organ thirst neurons. Computational modeling and experiments reveal that this circuit operates as a high-pass filter, selectively transmitting swallowing-evoked signals only when they occur in rapid succession, a characteristic of drinking. Our findings pinpoint the long-sought sensory origin of rapid thirst satiation and delineate the pharynx-to-forebrain circuit that transforms swallowing signal into drinking-specific inhibition to quench thirst.

10:00

The Crunchometer: A Low-Cost, Open-Source Acoustic Analysis Of Feeding Microstructure
Ranier Gutierrez
CINVESTAV del IPN, Mexico City, Mexico

Elucidating the neuronal circuits that govern appetite requires a detailed analysis of the microstructure of solid food consumption. A significant barrier in this field is that existing techniques for monitoring feeding are either prohibitively expensive, limiting their use, or lack the high temporal resolution necessary to align feeding events with neuronal activity. To overcome this, we developed the Crunchometer, a low-cost, open-source acoustic system that uses computational algorithms to create high-resolution feeding ethograms. We validated the system by monitoring feeding across different energy states (hunger/satiety) and by demonstrating that the anti-obesity drug semaglutide suppresses food intake and reduces preference for a high-fat diet. Crucially, the Crunchometer integrates seamlessly with in vivo neural recordings in freely behaving mice. By pairing our system with electrophysiology in the Lateral Hypothalamus (LH), we identified novel “meal-related” neurons that track entire meals rather than individual feeding bouts. Using calcium imaging, we further revealed that solid food consumption strongly modulates LH GABAergic and glutamatergic neurons. We also found that distinct LH neuronal ensembles encode the consumption of solid food versus liquid sucrose. The Crunchometer is thus a powerful and accessible tool for precisely dissecting the neural correlates of naturalistic feeding behavior.

10:30

Doing More With Less: Open-Source Tools Reveal Hidden Structure In Feeding And Motivation
Bridget Matikainen-Ankney
Rutgers University, Piscataway, NJ, United States

Open-source behavioral tools are fundamentally reshaping how we study ingestive behavior. Tools like FED3, FORCE, and home-cage activity monitoring systems are making the field more accessible, and generating data sets that are flexible and rich. These tools offer simple and adaptable methods to measure food-seeking and effort-based behaviors in a variety of experimental contexts. Assays using FED3 and FORCE, in particular, have been valuable for investigating motivated behaviors in mouse models of diet-induced obesity and weight loss. These platforms enable rapid data collection and efficiently allow iterative experimentation, which is particularly beneficial when establishing a research program. Another key strength of these tools is their ability to produce datasets that extend far beyond their initial applications. For instance, operant feeding assays with FED3 do more than track responses within a reinforcement schedule; they also capture the daily rhythms of feeding. Similarly, home-cage activity monitoring continuously records locomotion, which can then be analyzed alongside food-seeking behavior to uncover time-specific behavioral patterns that escape detection in traditional assays. The resulting datasets are complex, and can be mined again and again as new research questions arise. And while such rich datasets once posed analytical challenges, recent advances in analytical tools, especially those leveraging artificial intelligence, are breaking down such barriers, making sophisticated analyses accessible to all researchers, especially trainees. In sum, open-source tools are broadening access to behavioral neuroscience and enabling new lines of inquiry into feeding and motivation.

11:00

Ingestion On A Budget: Digital Mealtime Photography For Scalable Eating Behavior Assessment
Laura L Bellows
Cornell University, Ithaca, NY, United States

Measuring eating behaviors is often expensive, staff-intensive, and disconnected from real-world contexts, limiting scalability, particularly in low-resource populations. Digital food photography offers a cost-effective alternative that captures eating behaviors where they actually occur: at home. Prior work using the Remote Food Photography Method demonstrated feasibility among low-resource families, with 85% of expected dinner meal images captured and yielding rich contextual data on meal timing, preparation, and quality. Similarly, food photography in child care settings has enabled objective assessment of foods offered and consumed, revealing persistent gaps in diet quality (e.g., only 16% of packed lunches meeting nutrition guidelines) while reducing reliance on direct observation. Building on this foundation, we developed a mobile app–based mealtime photography tool that enables parents to capture before-and-after images of their child’s meals in real time. This approach reduces participant burden while generating objective data on foods offered, intake, and meal quality in the home environment. Pilot data demonstrate strong feasibility and engagement with repeated photo capture, supporting its use as a scalable assessment strategy. By shifting data collection from researchers to caregivers, digital food photography transforms assessment into a low-cost, scalable tool that can also support intervention delivery. This approach offers a practical pathway to expand access to behavioral nutrition interventions in resource-constrained settings and provides new insight into the context of eating behaviors beyond intake alone.

1:00

Assessment And Modification Of Ingestive Behavior As A Multi-Component Construct: Selecting The Best Method For The Population And Variable Of Interest
Corby Martin
Pennington Biomedical Research Center, Baton Rouge, , United States

Ingestive behavior is a multi-component construct encompassing several distinct behaviors and variables of interest. Various methods exist to assess ingestive behavior and these methods vary widely on their approach; assumptions; participant, researcher, or clinician burden; and incorporation of technology. Moreover, the validity of these methods varies widely, yet the validation data is not always consistent over different populations, endpoints of interest, or the state of participant (e.g., weight stable vs. weight unstable). This can result in selecting and using a dietary assessments method that is not suited for the variable of interest or the target population. These risks can be minimized, however, if we gain a better understanding of which aspect of ingestive behavior is the most relevant study or clinical outcome, and which methods are empirically supported to assess those outcomes in the population of interest. These issues will be reviewed during this talk and will include a critical review of assessing dietary and energy intake across the lifespan using a wide range of assessment methods, in addition to assessing meal frequency and meal timing via passive technology. Attendees will gain a better understanding of the strengths and weaknesses of dietary assessment methods based on what aspect of ingestive behavior is of interest and among which populations. Further, the review of assessment methods will include their ability to support modification of ingestive behaviors, including what and how much food is consumed, and when eating occurs. � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � ��

5:00 - 6:30 PM	Millennium Hall
Opening Reception & Exhibits

9:00 - 10:00 AM	Millennium Hall
Poster Session 1, Exhibits & Coffee Break

4:30 - 5:30 PM	On Own
Poster Session 2, Exhibits & Coffee Break

9:00 - 10:00 AM	Millennium Hall
Poster Session 3, Exhibits & Coffee Break

10:00 - 11:30 AM	Room 2
Symposium 2: Neuomodulation of Ingestive Behavior

9:00 - 10:00 AM	Millennium Hall
Poster Session 4, Exhibits & Coffee Break

2:00 - 3:00 PM	Millennium Hall
Poster Session 5, Exhibits & Coffee Break

3:00 - 4:30 PM	Room 2
Symposium 3: Gut Check: Mechanosensory Signals in Satiation

9:00 - 10:00 AM	Millennium Hall
Poster Session 6, Exhibits & Coffee Break

6:30 - 10:30 PM	Millennium Hall
Awards Ceremony & Closing Banquet

3:45 - 5:00 PM	Room 1
MARS Lecture 1: Camilla Nord

10:00 - 12:00 PM	Room 1
Presidential Symposium

12:00 - 1:30 PM	Room 1
Oral Session 1

12:00 - 1:30 PM	Room 2
Oral Session 2