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X-WR-CALNAME:Institute of Biomedical Engineering (BME)
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X-WR-CALDESC:Events for Institute of Biomedical Engineering (BME)
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DTSTART:20260308T070000
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DTSTART;TZID=America/Toronto:20260120T140000
DTEND;TZID=America/Toronto:20260120T150000
DTSTAMP:20260113T161123Z
CREATED:20251223T173420Z
LAST-MODIFIED:20260113T161123Z
UID:10000668-1768917600-1768921200@bme.utoronto.ca
SUMMARY:BME Faculty Member Search: Scott Tyler Albert: Expanding neural resilience to sensorimotor perturbations
DESCRIPTION:Brains are made to withstand disruption. When confronted by an external perturbation\, we seamlessly adapt our movement patterns to remain accurate and precise. Or when neural tissue dies\, our nervous system gradually adjusts to restore motor control. But this resilience is limited; whether in the face of an external disturbance\, or internal disorder\, we can never completely adapt\, sometimes leading to profound chronic impairment. To elucidate the cause of this ceiling on motor adaptation\, we will consider a model that treats adaptation as a balancing of error-based updating and obligatory forgetting. We will use this framework to design strategies that can boost the capacity of subconscious learning systems. Further\, we will explore how the presence of parallel systems for adaptation can alter the point at which learning saturates. Finally\, we will uncover the neural basis for motor recovery in a model of reaching and grasping in the rodent. Optogenetic perturbation to the sensorimotor cortex completely arrests the ability to move the limb\, but with repeated exposure\, a profound functional recovery presumes. To identify its source\, we will examine dynamics in key motor areas using invasive electrode recordings as well as functional MRI. Surprisingly\, we find that the restoration of behavior is supported by a network switching event\, where past centers of motor control are deactivated alongside a simultaneous recruitment of the intact cortex on the other side of the brain. \n\n\n\n \n\n\n\nAddress: Haultain Building\, (Rear of) 170 College Street*\, Room 410  \n\n\n\n*If entering through the main stairwell of the Mining Building\, there is a bridge that connects to the Haultain building at the 2nd level of the stairwell 
URL:https://bme.utoronto.ca/event/bme-faculty-member-search-scott-tyler-albert/
LOCATION:Haultain Building\, Room 410\, 170 College St\, Toronto\, M5S 3E3\, Canada
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BEGIN:VEVENT
DTSTART;TZID=America/Toronto:20260123T161000
DTEND;TZID=America/Toronto:20260123T162500
DTSTAMP:20260123T170749Z
CREATED:20251218T180622Z
LAST-MODIFIED:20260123T170749Z
UID:10000658-1769184600-1769185500@bme.utoronto.ca
SUMMARY:Graduate Student Seminar Series - Yu Qin
DESCRIPTION:Graduate Student Seminar Series\nPlease ensure you invite your Principal Investigator by adding their email via the ‘Add Guest’ button and they will also be notified of your presentation.\nLocation: 2nd Floor Auditorium (TRI/KITE) – 550 University Ave\nPresentation Title: A theory of pain chronification via maladaptive learning\nSupervisor Name: Steven Prescott\nYear of Study: 2\nProgram of Study: PhD\nReschedule Reason: Updating location information\nPowered by Calendly.com
URL:https://bme.utoronto.ca/event/graduate-student-seminar-series-yu-qin/
LOCATION:2nd Floor Auditorium (TRI/KITE)
CATEGORIES:Graduate Seminar Series
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=America/Toronto:20260123T162500
DTEND;TZID=America/Toronto:20260123T164000
DTSTAMP:20260123T170749Z
CREATED:20251218T180622Z
LAST-MODIFIED:20260123T170749Z
UID:10000657-1769185500-1769186400@bme.utoronto.ca
SUMMARY:Graduate Student Seminar Series - Vrushali Guruji
DESCRIPTION:Graduate Student Seminar Series\nPlease ensure you invite your Principal Investigator by adding their email via the ‘Add Guest’ button and they will also be notified of your presentation.\nLocation: 2nd Floor Auditorium (TRI/KITE) – 550 University Ave\nPresentation Title: Analyzing the Impact of Hemodynamics in Bicuspid Aortic Valve Disease Associated Ascending Aortic Dilatation\nAbstract: Bicuspid aortic valve (BAV) disease is characterized by two functioning leaflets instead of the normal three in a tricuspid aortic valve (TAV). Most BAV patients develop ascending aortic dilation (AAD)\, increasing their risk of fatal aortic dissection or rupture. We hypothesize that the elevated risk of developing AAD in BAV disease is a consequence of aberrant hemodynamics inducing gene perturbations in the aorta. To facilitate this investigation\, a novel mouse model with a mutation in the natriuretic peptide 2 receptor (Npr2) was employed\, enabling the isolation and evaluation of consequences accompanying aberrant blood flow. Notably\, though genetically identical\, 10% of Npr2+/- mice develop BAVs\, whereas the remaining 90% have TAVs. To expedite the progression of BAV-AAD\, mice are fed a high-fat western diet starting at 6 weeks of age. A novel echocardiogram protocol was developed to identify mice with BAVs or TAVs at 4 weeks of age\, prior to diet introduction (Guruji et al.\, 2024). Next\, the same echocardiogram protocol was performed on Npr2+/- mice at 6-weeks\, 4-months and 5-months of age. Echo-particle image velocimetry (echo-PIV) was also done to track the patterns of blood flow more accurately and identify flow impingement zones. At 5 months of age\, Npr2+/− mice with BAVs exhibited significantly elevated peak systolic velocities compared to TAV controls (2643 ± 392 vs. 1111 ± 146 mm/s\, P < 0.05). Consistent with pathological remodeling\, ascending aortic diameters were approximately 1.5-fold larger in Npr2+/−;BAV mice (1.75 ± 0.13 mm) compared to Npr2+/−;TAV mice (1.27 ± 0.01 mm)\, confirming BAV-associated AAD development. Aortic tissues from BAV and TAV mice were processed for spatial transcriptomic analysis using the Visium HD platform. Although data processing is ongoing\, preliminary analyses indicate differential expression of canonical dilation-associated genes in dilated Npr2+/−;BAV aortas relative to non-dilated Npr2+/−;TAV controls. Specifically\, COL1A1 expression was reduced in dilated aortas\, whereas ELN and ACTA2 expression was increased. Next steps involve integrating spatial transcriptomic data with echo-PIV-defined flow impingement maps to identify hemodynamically regulated gene expression signatures. Candidate genes will be validated by immunohistochemical staining in 5-month-old Npr2+/− BAV and TAV aortas. Together\, these studies aim to identify novel flow-dependent molecular drivers of AAD in BAV disease.\nSupervisor Name: Craig A. Simmons\nYear of Study: 4\nProgram of Study: PhD\nPowered by Calendly.com
URL:https://bme.utoronto.ca/event/graduate-student-seminar-series-vrushali-guruji-2/
LOCATION:2nd Floor Auditorium (TRI/KITE)
CATEGORIES:Graduate Seminar Series
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BEGIN:VEVENT
DTSTART;TZID=America/Toronto:20260123T164000
DTEND;TZID=America/Toronto:20260123T165500
DTSTAMP:20260123T170749Z
CREATED:20260107T185251Z
LAST-MODIFIED:20260123T170749Z
UID:10000673-1769186400-1769187300@bme.utoronto.ca
SUMMARY:Graduate Student Seminar Series - Yongzhi Guo
DESCRIPTION:Graduate Student Seminar Series\nPlease ensure you invite your Principal Investigator by adding their email via the ‘Add Guest’ button and they will also be notified of your presentation.\nLocation: 2nd Floor Auditorium (TRI/KITE) – 550 University Ave\nPresentation Title: An Image-Based Quantitative Platform to Study Metformin-Driven Adipocyte Metabolic Remodeling\nSupervisor Name: Alison McGuigan\nYear of Study: 2\nProgram of Study: MASc\nReschedule Reason: Updating location information\nPowered by Calendly.com
URL:https://bme.utoronto.ca/event/graduate-student-seminar-series-yongzhi-guo-2/
LOCATION:2nd Floor Auditorium (TRI/KITE)
CATEGORIES:Graduate Seminar Series
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