Amardeep Khushoo
Faculty VHT-FMRP (EBM, Scholarly Activity, QI-PS & Advocacy) at Valley Health Team, Inc.- Claim this Profile
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English -
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Hindi -
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Kashmiri Elementary proficiency
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Punjabi Limited working proficiency
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Bio
predman khushoo
very intelligent, sincere, disciplined and dedicated to his assignments ever since his school days.
predman khushoo
very intelligent, sincere, disciplined and dedicated to his assignments ever since his school days.
predman khushoo
very intelligent, sincere, disciplined and dedicated to his assignments ever since his school days.
predman khushoo
very intelligent, sincere, disciplined and dedicated to his assignments ever since his school days.
Credentials
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2020-2023 Disclosure of Unanticipated Outcomes
ECRIMay, 2023- Oct, 2024 -
Diabetes Quality Improvement Talks: Foundation of Change Course
ECRIMay, 2023- Oct, 2024 -
Patient Safety and Risk Management In The Physician Office: Culture of Safety
ECRIMay, 2023- Oct, 2024 -
Patient Safety and Risk Management In The Physician Office: Leadership and Event Reporting
ECRIMay, 2023- Oct, 2024 -
“The Chain of Infection: Know the Links, Break the Chain”
ECRIMay, 2023- Oct, 2024 -
Biomedical Responsible Conduct of Research Course 1.
CITI ProgramJun, 2022- Oct, 2024 -
Social and Behavioral Responsible Conduct of Research Course
CITI ProgramJun, 2022- Oct, 2024 -
Lean Six Sigma BLACK BELT in HEALTHCARE
Aveta Business InstituteOct, 2021- Oct, 2024 -
Ambulatory Care Clinical Risk Management Certification (Level 1-4)
ECRI InstituteAug, 2020- Oct, 2024 -
COVID-19 Contact Tracing
The Johns Hopkins UniversityMay, 2020- Oct, 2024 -
Basic Certificate in Quality & Safety
Institute for Healthcare Improvement (IHI) Open School - University of Minnesota ChapterAug, 2019- Oct, 2024 -
CITI Good Clinical Practice Course
CITI ProgramJun, 2022- Oct, 2024 -
Human Subjects Protection Training
CITI ProgramJun, 2022- Oct, 2024 -
Good Clinical Practice
The National Institute on Drug Abuse (NIDA)Apr, 2022- Oct, 2024
Experience
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Valley Health Team, Inc.
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United States
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Hospitals and Health Care
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1 - 100 Employee
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Faculty VHT-FMRP (EBM, Scholarly Activity, QI-PS & Advocacy)
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Sep 2018 - Present
Faculty at Valley Health Team Family Medicine Residency Program (VHT-FMRP) Faculty at Valley Health Team Family Medicine Residency Program (VHT-FMRP)
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COO/ Lab Director
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Aug 2012 - Present
• Director - Livestock Diagnostics Division. • Director - Pre-clinical & Biomarker testing (ELISA) for Contract Research. • Director - Livestock Diagnostics Division. • Director - Pre-clinical & Biomarker testing (ELISA) for Contract Research.
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ALTA FAMILY HEALTH CLINIC, INC.
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United States
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Hospitals and Health Care
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Research & Outreach Director
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Jan 2011 - Sep 2018
• Tele Medicine (Tele-Ophthalmology EyePACS program Director at ALTA with UC Berkeley) & Outreach. • Data analysis & generating reports for Tele-Dermatology at ALTA. • Tele Medicine (Tele-Ophthalmology EyePACS program Director at ALTA with UC Berkeley) & Outreach. • Data analysis & generating reports for Tele-Dermatology at ALTA.
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Postdoctoral Scientist
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Aug 2006 - Dec 2010
My primary focus was to develop a clinical assay to detect cystic fibrosis (CF), an autosomal inherited disease at the molecular level. Work was driven by critical need to develop an in vitro biochemical assay for screening for small corrector molecules that could potentially be used as a corrective drug in CF. Cystic fibrosis (CF) is caused by mutations in an ATP-gated chloride channel CFTR. The most common disease causing mutation, F508del, accounts for ~70% of the mutant alleles present… Show more My primary focus was to develop a clinical assay to detect cystic fibrosis (CF), an autosomal inherited disease at the molecular level. Work was driven by critical need to develop an in vitro biochemical assay for screening for small corrector molecules that could potentially be used as a corrective drug in CF. Cystic fibrosis (CF) is caused by mutations in an ATP-gated chloride channel CFTR. The most common disease causing mutation, F508del, accounts for ~70% of the mutant alleles present in humans. A major obstacle in understanding the primary defect caused by ∆F508 is that for CFTR, folding is initiated during synthesis while the nascent polypeptide is still tethered to the ribosome and thus is not amenable to traditional biochemical and biophysical approaches. We developed a FRET based approach that enabled us to study the folding of nascent ribosome-attached polypeptides at virtually any stage of synthesis. We have characterized the ‘NBD1 fold’ and in the process confirmed the finding that NBD1 folds co-translationally in cellular systems. Our study for the first time, has characterized an initial event in NBD1 folding i.e. formation of N-terminal ABC α/β sub-domain that acquires ATP binding competent fold quite early and even before the whole NBD1 domain synthesis is complete. We have proposed that it plays a role in stabilizing partially synthesized F1-type ATP-binding core sub-domain till the final fold is achieved. Further, we studied the cooperativity of the three sub-domains in the process of NBD1 folding. We have proposed that it plays a role in stabilizing partially synthesized F1-type ATP-binding core sub-domain till the final fold is achieved (See publications). I have also worked in collaboration with a colleague on project “Fluorescent analysis of de novo protein folding on (and off) the ribosome”. The findings of this project have been published in a peer reviewed journal, Journal of Biological Chemistry (JBC). Show less My primary focus was to develop a clinical assay to detect cystic fibrosis (CF), an autosomal inherited disease at the molecular level. Work was driven by critical need to develop an in vitro biochemical assay for screening for small corrector molecules that could potentially be used as a corrective drug in CF. Cystic fibrosis (CF) is caused by mutations in an ATP-gated chloride channel CFTR. The most common disease causing mutation, F508del, accounts for ~70% of the mutant alleles present… Show more My primary focus was to develop a clinical assay to detect cystic fibrosis (CF), an autosomal inherited disease at the molecular level. Work was driven by critical need to develop an in vitro biochemical assay for screening for small corrector molecules that could potentially be used as a corrective drug in CF. Cystic fibrosis (CF) is caused by mutations in an ATP-gated chloride channel CFTR. The most common disease causing mutation, F508del, accounts for ~70% of the mutant alleles present in humans. A major obstacle in understanding the primary defect caused by ∆F508 is that for CFTR, folding is initiated during synthesis while the nascent polypeptide is still tethered to the ribosome and thus is not amenable to traditional biochemical and biophysical approaches. We developed a FRET based approach that enabled us to study the folding of nascent ribosome-attached polypeptides at virtually any stage of synthesis. We have characterized the ‘NBD1 fold’ and in the process confirmed the finding that NBD1 folds co-translationally in cellular systems. Our study for the first time, has characterized an initial event in NBD1 folding i.e. formation of N-terminal ABC α/β sub-domain that acquires ATP binding competent fold quite early and even before the whole NBD1 domain synthesis is complete. We have proposed that it plays a role in stabilizing partially synthesized F1-type ATP-binding core sub-domain till the final fold is achieved. Further, we studied the cooperativity of the three sub-domains in the process of NBD1 folding. We have proposed that it plays a role in stabilizing partially synthesized F1-type ATP-binding core sub-domain till the final fold is achieved (See publications). I have also worked in collaboration with a colleague on project “Fluorescent analysis of de novo protein folding on (and off) the ribosome”. The findings of this project have been published in a peer reviewed journal, Journal of Biological Chemistry (JBC). Show less
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Oklahoma State University
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United States
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Higher Education
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700 & Above Employee
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Postdoctoral Research fellow
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2006 - Aug 2006
I was investigating mechanism of lamellar body exocytosis and surfactant secretion; role of SNARE’s and associated protein molecules in trafficking and fusion of these vesicles in alveolar epithelial type II cells. Briefly, I would culture primary cells (Rat lung alveolar epithelial cells; cell type I & II) in an air-liquid medium to maintain the phenotype of type II cells (which was technically challenging and expensive). In my short stay, I developed a system where we co-cultured type II… Show more I was investigating mechanism of lamellar body exocytosis and surfactant secretion; role of SNARE’s and associated protein molecules in trafficking and fusion of these vesicles in alveolar epithelial type II cells. Briefly, I would culture primary cells (Rat lung alveolar epithelial cells; cell type I & II) in an air-liquid medium to maintain the phenotype of type II cells (which was technically challenging and expensive). In my short stay, I developed a system where we co-cultured type II cells with immortalized cell lines such as - Rat type I-like alveolar epithelial cell line R3/1, fibroblast cell line in submerged culture conditions to mimic the lung epithelial lining. This technique not only helped immensely in maintaining the phenotype of type II cells but also enabled the lab to look at cell-cell communication between type I and type II alveolar epithelial cells. Show less I was investigating mechanism of lamellar body exocytosis and surfactant secretion; role of SNARE’s and associated protein molecules in trafficking and fusion of these vesicles in alveolar epithelial type II cells. Briefly, I would culture primary cells (Rat lung alveolar epithelial cells; cell type I & II) in an air-liquid medium to maintain the phenotype of type II cells (which was technically challenging and expensive). In my short stay, I developed a system where we co-cultured type II… Show more I was investigating mechanism of lamellar body exocytosis and surfactant secretion; role of SNARE’s and associated protein molecules in trafficking and fusion of these vesicles in alveolar epithelial type II cells. Briefly, I would culture primary cells (Rat lung alveolar epithelial cells; cell type I & II) in an air-liquid medium to maintain the phenotype of type II cells (which was technically challenging and expensive). In my short stay, I developed a system where we co-cultured type II cells with immortalized cell lines such as - Rat type I-like alveolar epithelial cell line R3/1, fibroblast cell line in submerged culture conditions to mimic the lung epithelial lining. This technique not only helped immensely in maintaining the phenotype of type II cells but also enabled the lab to look at cell-cell communication between type I and type II alveolar epithelial cells. Show less
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Education
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2006 - 2010
Oregon Health and Science University
Postdoctoral fellowship, Cystic Fibrosis/ Co-translational protein folding -
1999 - 2005
Center For Biotechnology, JNU, New Delhi
Doctor of Philosophy (PhD), Bioprocess & Genetic Engineering
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