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***CALL FOR ABSTRACTS***

2016 ACMT Annual Scientific Meeting Research Abstract Instructions and Online Submission

The ACMT is pleased to announce a CALL FOR RESEARCH ABSTRACTS for the 2016 Annual Scientific Meeting. 

Abstracts will be accepted September 15, 2015 until 11:59 pm Eastern Standard time on November 16, 2015.  Corresponding authors will be notified in mid-December 2015.

Instructions
Download instructions here.  Please read instructions carefully!
 
Examples of Submission Formatting (see instructions for details)
 
TITLE: 20 word limit
Required formatting: Efficacy of Trypsin in Treating Coral Snake Envenomation in the Porcine Model
Incorrect formatting: Efficacy of trypsin in treating coral snake envenomation in the porcine model 
 
ABSTRACT: 350 word limit  
Required formatting:

Background: Recent publications have identified that local anesthetics uncouple insulinergic signaling by inhibitiing pi3k/Akt and lipid emulsion activates Akt/GSK-3β following ischemia-reperfusion. Further, while it is clear that lipid emulsion exerts a cardiotonic effect, it is unclear through what pathway this effect functions.
Hypothesis: We hypothesized that bupivacaine uncouples insulinergic signaling which sensitizes the heart to insulinergic signaling during recovery (via feedback to IRS1) and lipid emulsion activates insulinergic signaling, potentiating the recovery effect.
Methods: Fourty-two male Sprague-Dawley rats received 10mg/kg Bupivacaine over 20s, followed by either nothing or 10mL/kg ILE (30% Intralipid®). Following sacrifice at 0 (control), 1.5, 5 or 10 minutes after start-of-infusion, heart, liver and kidney were frozen and/or preserved. An additional set of three animals was exposed to 10mL/kg ILE and sacrificed at the 5-minute time point; a final set of three animals was pre-treated with pi3k inhihitor Wortmannin, then subjected to 10mg/kg Bupivacaine and sacrificed at 10 minutes. Protein was extracted and phosphorylation level was quantified for Akt, p70, s6, IRS and Gsk-3β. Additional lysates were extracted for glycogen quantification. Tissue was also prepared for electron microscopy.
Results: High concentration bupivacaine blocked insulinergic signaling (in heart and kidney) via rapid de-phosphorylation of Akt/GSK-3β/p70/s6. Once drug concentration dropped below channel blocking thresholds, a rebound hyper-activation was observed. Blocking insulin signaling with Wortmannin exacerbated toxicity indicating the need for sensitization during recovery. Lipid treatment rapidly phosphorylated upstream insulingergic targets (Akt) with a delayed re-phosphorylation of downstream targets in insulin sensitive tissue (heart) but not in insulin-insensitive tissue (kidney). Further, in the absence of toxicity, lipid emulsion drove Akt phosphorylation. The sensitivity to insulin signaling was confirmed by increased glycogen accumulation in lipid treatment using both biochemical assay and electron microscopy.
Discussion: Bupivacaine toxicity blocks insulinergic signaling and the sensitization to insulin-signaling via IRS1 de-phosphorylation is required for recovery. Lipid emulsion potentiates the recovery by its ability to drive insulinergic signaling in the absence of toxicity.
Conclusion: In addition to its ability to sequester toxins, the benefit of lipid emulsion in combatting cardiac toxicity may be modulated its pro-insulinergic effect

_____________________________
Incorrect formatting:  

Background: Recent publications have identified that local anesthetics uncouple insulinergic signaling by inhibitiing pi3k/Akt and lipid emulsion activates Akt/GSK-3β following ischemia-reperfusion. Further, while it is clear that lipid emulsion exerts a cardiotonic effect, it is unclear through what pathway this effect functions. Hypothesis: We hypothesized that bupivacaine uncouples insulinergic signaling which sensitizes the heart to insulinergic signaling during recovery (via feedback to IRS1) and lipid emulsion activates insulinergic signaling, potentiating the recovery effect. Methods: Fourty-two male Sprague-Dawley rats received 10mg/kg Bupivacaine over 20s, followed by either nothing or 10mL/kg ILE (30% Intralipid®). Following sacrifice at 0 (control), 1.5, 5 or 10 minutes after start-of-infusion, heart, liver and kidney were frozen and/or preserved. An additional set of three animals was exposed to 10mL/kg ILE and sacrificed at the 5-minute time point; a final set of three animals was pre-treated with pi3k inhihitor Wortmannin, then subjected to 10mg/kg Bupivacaine and sacrificed at 10 minutes. Protein was extracted and phosphorylation level was quantified for Akt, p70, s6, IRS and Gsk-3β. Additional lysates were extracted for glycogen quantification. Tissue was also prepared for electron microscopy. Results: High concentration bupivacaine blocked insulinergic signaling (in heart and kidney) via rapid de-phosphorylation of Akt/GSK-3β/p70/s6. Once drug concentration dropped below channel blocking thresholds, a rebound hyper-activation was observed. Blocking insulin signaling with Wortmannin exacerbated toxicity indicating the need for sensitization during recovery. Lipid treatment rapidly phosphorylated upstream insulingergic targets (Akt) with a delayed re-phosphorylation of downstream targets in insulin sensitive tissue (heart) but not in insulin-insensitive tissue (kidney). Further, in the absence of toxicity, lipid emulsion drove Akt phosphorylation. The sensitivity to insulin signaling was confirmed by increased glycogen accumulation in lipid treatment using both biochemical assay and electron microscopy. Discussion: Bupivacaine toxicity blocks insulinergic signaling and the sensitization to insulin-signaling via IRS1 de-phosphorylation is required for recovery. Lipid emulsion potentiates the recovery by its ability to drive insulinergic signaling in the absence of toxicity. Conclusion: In addition to its ability to sequester toxins, the benefit of lipid emulsion in combatting cardiac toxicity may be modulated its pro-insulinergic effect.

 
 Author:
Required formatting:   Smith AB 
Incorrect formatting:  Adam B Smith

Click here to submit an abstract (Deadline: November 16, 2015)

If you have questions concerning the online submission platform contact info@acmt.net.