Difference between revisions of "Ian C Salveson"

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You have reached the personal page of Styles Bitchly.
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You have reached the personal page of Ian Salveson.
  
 
==Personal Information==
 
==Personal Information==
Junior Chemistry and Classics Major
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Senior Chemistry and Classics Major
  
 
Hometown: St. Charles, IL
 
Hometown: St. Charles, IL
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Spring 2016: Chem 430 with B. Sturgeon
 
Spring 2016: Chem 430 with B. Sturgeon
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Summer 2016: Kieft Summer Research with Brad Sturgeon (Acetaminophen Oxidation)
  
 
==Presentations==
 
==Presentations==
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Poster Title: ''Enzymatic Oxidation of Acetaminophen''
 
Poster Title: ''Enzymatic Oxidation of Acetaminophen''
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July 2016: '''Kieft Summer Research Presentations'''
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Title: Oxidation of Biophenols
  
 
==Interests==
 
==Interests==
  
Water Polo
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-Water Polo
Cooking
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-Cooking
Magic: The Gathering
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-Magic: The Gathering
  
 
==Career Plans==
 
==Career Plans==
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==Projects==
 
==Projects==
  
'''The Mechanism of Acetaminophen Metabolism'''  
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[[Acetaminophen Oxidation|'''The Mechanism of Acetaminophen Metabolism''']]
  
 
Acetaminophen, also known as paracetamol, is a commonly used over-the-counter pain reliever. It is also present in mixtures of prescribed pain medication. Taken in accordance with dosage suggestions, acetaminophen is processed normally by the body and does not cause any adverse side effects; however, taken in excess, acetaminophen can quickly lead to liver failure and death. Acetaminophen alone is responsible for 50% of transplants due to drug related liver injury. Correct identification of the mechanism of acetaminophen induced liver damage is the first step in treating and preventing acetaminophen related liver failure. The currently accepted mechanism for liver injury due to acetaminophen involves the creation of a highly reactive oxidation product NAPQI. However, research has identified the formation of a radical during the enzymatic oxidation of acetaminophen. This has led to a new hypothesis where radicals are continuously forming and combining into polymeric material that would cause a buildup of insoluble material within the liver, preventing blood flow and leading to necrosis. This research will revolve around investigating this new hypothesis by analyzing the products of controlled enzymatic oxidations of acetaminophen using HPLC alongside with NMR and Mass Spectroscopy for the characterization of these products.
 
Acetaminophen, also known as paracetamol, is a commonly used over-the-counter pain reliever. It is also present in mixtures of prescribed pain medication. Taken in accordance with dosage suggestions, acetaminophen is processed normally by the body and does not cause any adverse side effects; however, taken in excess, acetaminophen can quickly lead to liver failure and death. Acetaminophen alone is responsible for 50% of transplants due to drug related liver injury. Correct identification of the mechanism of acetaminophen induced liver damage is the first step in treating and preventing acetaminophen related liver failure. The currently accepted mechanism for liver injury due to acetaminophen involves the creation of a highly reactive oxidation product NAPQI. However, research has identified the formation of a radical during the enzymatic oxidation of acetaminophen. This has led to a new hypothesis where radicals are continuously forming and combining into polymeric material that would cause a buildup of insoluble material within the liver, preventing blood flow and leading to necrosis. This research will revolve around investigating this new hypothesis by analyzing the products of controlled enzymatic oxidations of acetaminophen using HPLC alongside with NMR and Mass Spectroscopy for the characterization of these products.

Latest revision as of 19:01, 21 July 2016

You have reached the personal page of Ian Salveson.

Personal Information

Senior Chemistry and Classics Major

Hometown: St. Charles, IL

Undergraduate Research Activities

Summer 2015: Kieft Summer Research with Brad Sturgeon (Acetaminophen Oxidation)

Spring 2016: Chem 430 with B. Sturgeon

Summer 2016: Kieft Summer Research with Brad Sturgeon (Acetaminophen Oxidation)

Presentations

June 2014: Kieft Summer Research Presentations

Title: A Simulated Study of Acetaminophen Induced Liver Injury

March 2016: 251th National ACS Meeting San Diego, CA

Poster Title: Enzymatic Oxidation of Acetaminophen

July 2016: Kieft Summer Research Presentations

Title: Oxidation of Biophenols

Interests

-Water Polo -Cooking -Magic: The Gathering

Career Plans

College Chemistry Professor

Projects

The Mechanism of Acetaminophen Metabolism

Acetaminophen, also known as paracetamol, is a commonly used over-the-counter pain reliever. It is also present in mixtures of prescribed pain medication. Taken in accordance with dosage suggestions, acetaminophen is processed normally by the body and does not cause any adverse side effects; however, taken in excess, acetaminophen can quickly lead to liver failure and death. Acetaminophen alone is responsible for 50% of transplants due to drug related liver injury. Correct identification of the mechanism of acetaminophen induced liver damage is the first step in treating and preventing acetaminophen related liver failure. The currently accepted mechanism for liver injury due to acetaminophen involves the creation of a highly reactive oxidation product NAPQI. However, research has identified the formation of a radical during the enzymatic oxidation of acetaminophen. This has led to a new hypothesis where radicals are continuously forming and combining into polymeric material that would cause a buildup of insoluble material within the liver, preventing blood flow and leading to necrosis. This research will revolve around investigating this new hypothesis by analyzing the products of controlled enzymatic oxidations of acetaminophen using HPLC alongside with NMR and Mass Spectroscopy for the characterization of these products.

Experiments

Flash Chromatography(2/15/2016)