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Effects of Dexmedetomidine Administr...

Gregory, Anastacia.

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Effects of Dexmedetomidine Administration on Drosophila melanogaster with Leigh Syndrome.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Effects of Dexmedetomidine Administration on Drosophila melanogaster with Leigh Syndrome./
Author:	Gregory, Anastacia.
other author:	Lisle, Chelsie
Published:	Ann Arbor : ProQuest Dissertations & Theses, : 2021,
Description:	86 p.
Notes:	Source: Dissertations Abstracts International, Volume: 82-06, Section: B.
Contained By:	Dissertations Abstracts International82-06B.
Subject:	Genetics. -
Online resource:	https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=28156197
ISBN:	9798698500650

Effects of Dexmedetomidine Administration on Drosophila melanogaster with Leigh Syndrome.
Gregory, Anastacia.

Effects of Dexmedetomidine Administration on Drosophila melanogaster with Leigh Syndrome. - Ann Arbor : ProQuest Dissertations & Theses, 2021 - 86 p.

Source: Dissertations Abstracts International, Volume: 82-06, Section: B.

Thesis (Ph.D.)--Webster University, 2021.

This item must not be sold to any third party vendors.

Mitochondrial disease (MD) encompasses disease states that are a result of alterations in mitochondrial proteins, originating from either nuclear (n) or mitochondrial (mt) DNA mutations. These alterations may affect either the oxidative phosphorylation system (OXPHOS) or other non-energy producing functions of the organelle. MD umbrellas the unwarranted presentation of neurological, respiratory, cardiac, musculoskeletal, and endocrine disorders. Cells in these systems have a high demand for energy and therefore contain many mitochondria. Anesthetic medications target these same systems. The use of anesthetic agents in combination with MD exposes such individuals to perioperative complications. Currently, there are not well-controlled quantitative research studies that have tested the effects of commonly used anesthetic agents on patients with a known MD. Most research on MD and the relation to anesthetic agents is performed on model organisms. There have been numerous case reports that have described the safe anesthetic use of dexmedetomidine (DEX) within this patient population. This study examined the physiological effects of DEX in Drosophila (D) melanogaster with Leigh syndrome (LS). This research determined that after the acute and chronic administration of DEX to two different strains (NDB8 and SURF1) of D. melanogaster with LS, there was no effect on heart rate. Methods: This study used a quantitative laboratory research design in order to analyze larval heart rates after the administration of dose dependent DEX. Experimental groups included D. melanogaster with global gene knockdown in either NDB8 or SURF1 genes that were exposed to DEX. There were four control groups including, Wild Type (WT)no treatment, WT with treatment, NDB8 no treatment, and SURF1 no treatment. The extent of gene expression was confirmed statistically with the use of real time PCR. Results: A One-way ANOVA showed significance after acute exposure of DEX (p = 0. 0001) in WT vs. NDB8 or SURF1 strains (124, 74, and 94, respectively). However, a Tukey's Test determined there was no significance between relevant control and treatment groups (p > 0. 05). When statistically compared, there was no significance between WT vs. NDB8 or SURF1 (n = 60 for each group) after chronic exposure to DEX. To confirm the amount of expressed gene knockdown, there was significance in the amount of SURF1 RNAi expression when compared to WT RNA (p = 0. 0131). However, there was no significance in the NDB8 RNAi expression when compared to WT RNA (p = 0. 2074). Conclusion: It can be concluded that acute and chronic administration of DEX has no effect on larval heart rates of D. melanogaster with genetically predisposed global knockdown of the NDB8 or SURF1 gene; two common genetic variations seen in LS. The hypothesis, dose dependently administered DEX will have no effect on heart rate in D. melanogaster with LS is accepted. It is reasonable to consider DEX as a choice anesthetic agent for this patient population as it has not yet been proven to suppress mitochondrial function, has neuroprotective properties, and does not suppress respiratory drive.

ISBN: 9798698500650Subjects--Topical Terms:

530508
Genetics.
Subjects--Index Terms:

Anesthesia

Effects of Dexmedetomidine Administration on Drosophila melanogaster with Leigh Syndrome.
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300 $a 86 p.
500 $a Source: Dissertations Abstracts International, Volume: 82-06, Section: B.
500 $a Advisor: Schroeder, Stephanie;Curdt, Nicholas.
502 $a Thesis (Ph.D.)--Webster University, 2021.
506 $a This item must not be sold to any third party vendors.
520 $a Mitochondrial disease (MD) encompasses disease states that are a result of alterations in mitochondrial proteins, originating from either nuclear (n) or mitochondrial (mt) DNA mutations. These alterations may affect either the oxidative phosphorylation system (OXPHOS) or other non-energy producing functions of the organelle. MD umbrellas the unwarranted presentation of neurological, respiratory, cardiac, musculoskeletal, and endocrine disorders. Cells in these systems have a high demand for energy and therefore contain many mitochondria. Anesthetic medications target these same systems. The use of anesthetic agents in combination with MD exposes such individuals to perioperative complications. Currently, there are not well-controlled quantitative research studies that have tested the effects of commonly used anesthetic agents on patients with a known MD. Most research on MD and the relation to anesthetic agents is performed on model organisms. There have been numerous case reports that have described the safe anesthetic use of dexmedetomidine (DEX) within this patient population. This study examined the physiological effects of DEX in Drosophila (D) melanogaster with Leigh syndrome (LS). This research determined that after the acute and chronic administration of DEX to two different strains (NDB8 and SURF1) of D. melanogaster with LS, there was no effect on heart rate. Methods: This study used a quantitative laboratory research design in order to analyze larval heart rates after the administration of dose dependent DEX. Experimental groups included D. melanogaster with global gene knockdown in either NDB8 or SURF1 genes that were exposed to DEX. There were four control groups including, Wild Type (WT)no treatment, WT with treatment, NDB8 no treatment, and SURF1 no treatment. The extent of gene expression was confirmed statistically with the use of real time PCR. Results: A One-way ANOVA showed significance after acute exposure of DEX (p = 0. 0001) in WT vs. NDB8 or SURF1 strains (124, 74, and 94, respectively). However, a Tukey's Test determined there was no significance between relevant control and treatment groups (p > 0. 05). When statistically compared, there was no significance between WT vs. NDB8 or SURF1 (n = 60 for each group) after chronic exposure to DEX. To confirm the amount of expressed gene knockdown, there was significance in the amount of SURF1 RNAi expression when compared to WT RNA (p = 0. 0131). However, there was no significance in the NDB8 RNAi expression when compared to WT RNA (p = 0. 2074). Conclusion: It can be concluded that acute and chronic administration of DEX has no effect on larval heart rates of D. melanogaster with genetically predisposed global knockdown of the NDB8 or SURF1 gene; two common genetic variations seen in LS. The hypothesis, dose dependently administered DEX will have no effect on heart rate in D. melanogaster with LS is accepted. It is reasonable to consider DEX as a choice anesthetic agent for this patient population as it has not yet been proven to suppress mitochondrial function, has neuroprotective properties, and does not suppress respiratory drive.
590 $a School code: 0813.
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650 4 $a Biology. $3 522710
650 4 $a Pharmacology. $3 634543
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653 $a Mitochondrial disease
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