BME
Monday ROUNDTABLE
JUNE
21, 2023
DEPUTY
HEAD’S NOTE
I
hope everything has a good summer so far and enjoyed the time off with family and friends. To many of us, including me, who are proud of fatherhood, I hope you enjoyed the Father’s Day weekend and perhaps the US Open golf.
UPCOMING
IMPORTANT DATES
Week
of June 19
Wed.,
June 21: BME
Summer Seminar Series,
9:30
a.m. via Zoom. Madeline McLaughlin (Carmela Evans-Molina/Fang Huang, advisors) will present “STIM1 Interacts with G Protein-Coupled Estrogen Receptor Signaling to Maintain â Cell Identity in Female Mice”
and Shatha Mufti (Riyi Shi, advisor) will present “Assessment of Seizure-Like Activity in Neuronal Networks Post-Traumatic Brain Injury Utilizing Novel TBI-On-A-Chip Model.”
Upcoming
Opportunity for Fun!
Do
you play a band instrument? Purdue
Bands and Orchestras has just opened registration for the 2023 Purdue University Summer Band!
This ensemble is open to all area musicians that are high school age and up. Participation in Purdue’s Summer Band is FREE to all. We plan to begin rehearsals on Tuesday, June 20, and rehearse on Tuesday and Thursday afternoons from
4:00-5:30 PM in Hagle Hall, Room 178. Our concert will be held on Thursday, July 20, 6:30 PM at Columbian Park Memorial Island Amphitheater immediately prior to a performance by the Lafayette Citizens' Band.
Register
Here: https://docs.google.com/forms/d/e/1FAIpQLSd8v47EEuzyl070XPk4QyH0fIBflpdLywlCfrGKLKZTtr4Stw/viewform
Upcoming
important deadlines and info.
Mon.,
July 24: Final Grade Entry Begins. (Ends
promptly at 5:00 p.m., Tues., August 8th).
Wed.,
Sept. 6: BMES
Early Bird Registration Deadline! Register
now to lock in savings with early-bird pricing for the 2023 BMES Annual Meeting (to be held in Seattle, WA, October 11-14). Thousands of biomedical engineers will attend this year’s meeting to learn, collaborate, and network. As a BMES member, you can save
more than 10% with reduced early bird rates, so if you’re not already a member, now would be a good time to join! Click here for details:
https://mailchi.mp/e3958bb463f2/o8cvhb9q5x-9335625?e=ea10e317a2
NOTE:
We recommend booking your room at the Hyatt Regency Seattle because it’s
closer to the convention center AND it’s where university receptions will be held (in addition to some being held
inside the convention center). Here’s the link to reserve with the $259 discount rate.
This rate only lasts until the allotted number of rooms have been sold.
https://www.hyatt.com/en-US/group-booking/SEARS/G-BMES
Committee
Updates
Academic
Programs Update
Summer
Grading Deadlines:
Graduate
Office Update
Resources
and further information
BME Summer Seminar Series,
Wed., June 21,
9:30 a.m. via Zoom.
Madeline McLaughlin (Carmela Evans-Molina/Fang Huang, advisors) will present “STIM1 Interacts with G Protein-Coupled Estrogen Receptor Signaling to Maintain â Cell Identity in Female Mice”
and Shatha Mufti (Riyi Shi, advisor) will present “Assessment of Seizure-Like Activity in Neuronal Networks Post-Traumatic Brain Injury Utilizing Novel TBI-On-A-Chip Model.”
STIM1 Interacts with G Protein-Coupled Estrogen Receptor Signaling to Maintain â Cell Identity in Female Mice
Abstract:
Calcium (Ca2+) plays a vital role in normal pancreatic â cell function, and the â cell endoplasmic reticulum (ER) serves as the dominant intracellular store of Ca2+. ER Ca2+ depletion triggers a rescue mechanism known as
store-operated Ca2+ entry (SOCE), which replenishes ER Ca2+ stores through the ER-localized Ca2+ sensor stromal interaction molecule 1 (STIM1). We have demonstrated pathogenic reductions in â cell SOCE and loss of STIM1 expression
in rodent and human models of type 2 diabetes (T2D) and shown that â cell-specific loss of STIM1 (STIM1Äâ) leads to obesity-induced glucose intolerance, decreased â cell and increased
cell mass in female but not male STIM1Äâ mice. RNA sequencing of islets isolated from female STIM1Äâ mice revealed reductions in G-protein coupled estrogen receptor (GPER) expression and a transcriptional signature indicative of reduced estradiol mediated
signaling. To test whether GPER is required for the maintenance of â cell identity, INS-1 cells were transfected with siRNA targeted to
Gper1 or treated with the GPER1 antagonist, G-15. RT-qPCR showed that markers of â cell identity were significantly reduced and
Gcg expression was significantly increased in Gper1 knockdown and G-15-treated cells. Lastly, to determine the relationship between estradiol signaling and â cell identity, we performed ovariectomy surgeries in female mice and showed that loss
of estradiol signaling leads to obesity-induced glucose intolerance. Further experiments are warranted to determine the differentiation status of the â cells in the ovariectomized mice and the mechanisms behind this connection. Together, these data identify
a novel connection between â cell SOCE, GPER signaling, and â cell differentiation status.
Evaluation link for Madeline McLaughlin:
https://purdue.ca1.qualtrics.com/jfe/form/SV_b7b3MGYdztRV7gy
Assessment of Seizure-Like Activity in Neuronal Networks Post-Traumatic Brain Injury Utilizing Novel TBI-On-A-Chip Model
Abstract: Traumatic brain injury (TBI) is a leading cause of death and long-term disability worldwide. Further, seizure development
is one of the most serious sequalae post-TBI. Unfortunately, the underlying mechanisms connecting TBI and seizures are not well understood. Identifying cell-scale pathophysiological changes in the brain post-injury will be paramount for identifying therapeutic
targets. Cell membrane damage, which results from the uncontrollable cell stretching upon injury, is considered one of the main causes of cellular ionic imbalances and biochemical changes that can lead to the deterioration of TBI cases. Membrane permeability
changes caused by membrane breaches may increase the susceptibility of cells to seizure-like activity (SLA) with increased cell depolarization. Furthermore, as neuronal networks try to reorganize around the injury site, hyperexcitability of networks may result,
which leads to increased seizure susceptibility. Polyethylene glycol (PEG), a hydrophilic polymer and known fusogen, has shown potential in sealing damaged cell membranes and restoring functional recovery post-TBI in preclinical studies. Therefore, we hypothesize
that targeting cell membrane damage therapeutically with PEG would mitigate the reduction in seizure initiation threshold post-TBI. Investigation of PEG treatment effects would be carried out in our unique TBI-on-a-chip system, which simulates the pathophysiology
of concussive TBI by applying clinically relevant, rapid acceleration injuries to murine cortical networks on custom microelectrode arrays, while providing real-time, cell-scale monitoring of electrophysiological and morphological changes. Utilizing extracellular
recordings of network spike activity, we reveal the spontaneous appearance of SLA in networks exposed to 10 rapidly (4-6 sec) administered 30 g impacts. Furthermore, we attempt to better characterize SLA and burst features to gain critical information about
post-injury electrophysiological changes. In summary, our TBI-on-a-chip model could provide vital insights into functional and morphological changes post-TBI, while enabling the investigation of underlying SLA mechanisms, which could lead to the identification
of potential therapeutic targets.
Evaluation link for Shatha Mufti:
https://purdue.ca1.qualtrics.com/jfe/form/SV_bqtEefXLhwxHdDE
*Join Zoom Meeting
https://purdue-edu.zoom.us/j/98231659969?pwd=T21Oa1B6QzFyQzFvckMzS1doNGlJUT09
Meeting ID: 982 3165 9969 Passcode: biomedical
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