Innovative spinal cord protection with endogenous, cytoprotective, heat shock protein 70i nanotechnology in aortic pathology.
Presented During:
Thursday, April 25, 2024: 5:38PM - 7:00PM
Sheraton Times Square
Posted Room Name:
Central Park
Abstract No:
P0176
Submission Type:
Abstract Submission
Authors:
Barbara Robinson (1), Hartzell Schaff, MD (2)
Institutions:
(1) Your Health Llc, Lake Barrington, IL, (2) Mayo Clinic, Rochester, MN
Submitting Author:
Barbara Robinson
-
Contact Me
Your Health Llc
Your Health Llc
Co-Author:
*Hartzell Schaff, MD
-
Contact Me
Mayo Clinic
Mayo Clinic
Presenting Author:
Barbara Robinson
-
Contact Me
Br health for you llc
Br health for you llc
Abstract:
Introduction. I had a vision, applied scholarship with leader ship regarding endogenous, neurologic
Spinal cord ischemia, paresis, paraparesis, paralysis, while rare, are all major problems fraught with support structure Most work has focused on exogenous means to protect the spinal cord. No data exists on ENDOGENOUS heat shock proteins to protect against spinal cord ischemia .
Our lab has extensive experience with hsp70i induction in various animal models. We have previously induced myocardial hsp70i resulting in doubling recovery of myocardial function preload recruitable work area after stunning. Also we induced coronary artery hsp70i result in improved coronary artery peak flow and coronary relaxation. This was also predominantly due to induction in the nuclear fraction in both the myocardium as well as coronary artery.
(Figure.)
No one has previously examined if HSP 70 can be induced in the descending aorta. The descending aorta and multiple factors affect spinal cord. Often times in the clinical scenario, spinal cord paresis or paralysis, are not necessarily evident until 24 to 48 hours after the insult and having heat shock protein present during this time period is more ideal.
In order to achieve this, dogs underwent hyperthermic or normothermic bypass and aortic hsp70 was examined at either 12 or 24 hours after hyperthermia. After either 12 or 24 hours, the descending aorta was harvested and frozen at -70° until further analysis was performed. Once sufficient number of aorta were obtained at 12 hours and 24 hours and subject to western blot analysis. The HSP 70 anybody was obtained from Stressgen.
AIM
Through vision leadership and scholarship, we proposed HSP 70 could be induced in the descending aorta with heat stress for potential protection against paralysis.
Results
Experimentation reveals that hyperthermia can induce hsp 70 within the descending aorta. Hsp70 is greater at 24 hours after hyperthermia than at 12 hours. The relative amounts of nuclear to cytoplasmic fraction is also greater at 24 hours than 12 hours. This is clinically important given that the sequelae resulting in spinal cord ischemia after any aortic procedure generally presents at 24 to 48 hours after aortic ischemia.
Discussion
All humans make endogenous hsps.There a paucity research on aortic hsps and spinal cord protection. Were the first to demonstrate that aorta hsp70 can be upregulated and at different time points with increased nuclear to cytoplasmic fractions. This has significant clinical sequelae as later increase in hsps has clinical benefit when potential spinal cord is most likely to occur after aortic surgery or stentibg.
Further mechanisms of hsp70 protection, remain to be investigated; this may involve antiapoptotic mechanisms such as mitochondria protection. Recent rapid advances in nanotechnology and newer agents, such as geranylgeranyl acetone, offer new opportunities for therapy against the aging diseased aorta.
Spinal cord ischemia, paresis, paraparesis, paralysis, while rare, are all major problems fraught with support structure Most work has focused on exogenous means to protect the spinal cord. No data exists on ENDOGENOUS heat shock proteins to protect against spinal cord ischemia .
Our lab has extensive experience with hsp70i induction in various animal models. We have previously induced myocardial hsp70i resulting in doubling recovery of myocardial function preload recruitable work area after stunning. Also we induced coronary artery hsp70i result in improved coronary artery peak flow and coronary relaxation. This was also predominantly due to induction in the nuclear fraction in both the myocardium as well as coronary artery.
(Figure.)
No one has previously examined if HSP 70 can be induced in the descending aorta. The descending aorta and multiple factors affect spinal cord. Often times in the clinical scenario, spinal cord paresis or paralysis, are not necessarily evident until 24 to 48 hours after the insult and having heat shock protein present during this time period is more ideal.
In order to achieve this, dogs underwent hyperthermic or normothermic bypass and aortic hsp70 was examined at either 12 or 24 hours after hyperthermia. After either 12 or 24 hours, the descending aorta was harvested and frozen at -70° until further analysis was performed. Once sufficient number of aorta were obtained at 12 hours and 24 hours and subject to western blot analysis. The HSP 70 anybody was obtained from Stressgen.
AIM
Through vision leadership and scholarship, we proposed HSP 70 could be induced in the descending aorta with heat stress for potential protection against paralysis.
Results
Experimentation reveals that hyperthermia can induce hsp 70 within the descending aorta. Hsp70 is greater at 24 hours after hyperthermia than at 12 hours. The relative amounts of nuclear to cytoplasmic fraction is also greater at 24 hours than 12 hours. This is clinically important given that the sequelae resulting in spinal cord ischemia after any aortic procedure generally presents at 24 to 48 hours after aortic ischemia.
Discussion
All humans make endogenous hsps.There a paucity research on aortic hsps and spinal cord protection. Were the first to demonstrate that aorta hsp70 can be upregulated and at different time points with increased nuclear to cytoplasmic fractions. This has significant clinical sequelae as later increase in hsps has clinical benefit when potential spinal cord is most likely to occur after aortic surgery or stentibg.
Further mechanisms of hsp70 protection, remain to be investigated; this may involve antiapoptotic mechanisms such as mitochondria protection. Recent rapid advances in nanotechnology and newer agents, such as geranylgeranyl acetone, offer new opportunities for therapy against the aging diseased aorta.
Aortic Symposium:
Spinal Cord Protection
Image or Table
Presentation
