Patrick L. Gentry
- Courses10
- Reviews24
- School: Indiana University
- Campus: Purdue University Indianapolis
- Department: Biology
- Email address: Join to see
- Phone: Join to see
-
Location:
420 University Blvd
Indianapolis, IN - 46202 - Dates at Indiana University: May 2016 - May 2020
- Office Hours: Join to see
N/A
Would take again: Yes
For Credit: Yes
0
0
Not Mandatory
Awesome
Professor Gentry is a cool guy. He's straightforward in his lectures. He will provide you information, but still in an intriguing way. There were several group projects. However, nothing in his class has ever been overwhelming. Overall, he's very nice and he made this class easy.
Biography
Indiana University Purdue University Indianapolis - Biology
Lecturer and Instructional Coordinator, Department of Biology
Education Management
Patrick
Gentry, PhD
Indianapolis, Indiana
I am currently a Lecturer in the Department of Biology, School of Science at IUPUI. I am an Instructional Coordinator, an administrator of the First-Year Science Apprenticeship in Biology program, and Instructor for N107: Intro to the World of Animals, N322: Intro to the Principal of Genetics, T585: Model Organisms in Research (100% online), and Biology Summer Bridge.
In my current position, I have experience managing a $100,000 grant that is used to hire first-year students to work in the biology department as part of the First -year Science Apprenticeship program. In addition to keeping track of the budget, I am responsible for hiring, placing, and keeping track of apprentice time sheets. I have experience writing proposals and grants. In the past year, I have written and won the Course Enhancement Grant from the Center for Teaching and Learning. I am in the process of finishing writing a $20,000 grant proposal that incorporates faculty, students, and ideas from several departments to the STEM Education Innovation and Research Institute, that will develop a new research-based course that partners with local museums and state environmental agencies. Much of my work has been based on the need to develop relationships and inspire cooperation through transformational leadership. In 2009-10, I started a Not-for-Profit and team of educators, attorneys, and neighborhood associations, and developed a proposal for an Indianapolis Mayor Sponsored Charter School. Our team was able to get the support of Purdue University’s Extension Education Office. We put forth a solid proposal, however, we were not selected for a charter. In addition to these examples, I have had to work in non-traditional settings with great autonomy. This is demonstrated in my early career as a paramedic, where quick evaluation, teamwork, and sound decision making was needed in order to treat and transfer patients to the appropriate hospital setting.
Experience
MSD Wayne Township
Science Teacher
Project-Based Learning Team Representative
Cooperative Learning Training TeamThe Alchemy Project: Forging the Elements of Hope, Desire, and SuccessTM
President
Not-for-profit with the purpose of educating and providing education opportunities for children of poverty and under represented groups in the field of science.
GEO Foundation
Science Teacher
Patrick worked at GEO Foundation as a Science Teacher
Zionsville Community Schools
AP Chemistry Teacher
Patrick worked at Zionsville Community Schools as a AP Chemistry Teacher
School of Science at IUPUI
Lecturer, Instructional Coordinator
Instructor of N107: Intro to the World of Animals
N322: Intro to the Principal of Genetics
T585: Model Organisms in Research (100% online)
Biology Summer Bridge
Curriculum Enhancement Grant Recipient 2018
Writing Curriculum
Administration of Work Study Program
Scheduling and Assigning Laboratory Instruction
Mentor and Coordinate TA Instructors
Laboratory Instruction
Education
Indiana University School of Medicine
Master's
Cellular and Integrative Physiology
Purdue University
Doctor of Philosophy (Ph.D.)
Educational Leadership and Administration, General
Publications
DAPK mediates TNF-alpha induced apoptosis by TNF-receptor 1 association and JNK activation through MKK7 (Meeting Abstract)
The FASEB Journal
Death Associated Protein Kinase (DAPK) is a calcium calmodulin (CaM) regulated serine/threonine kinase, which has a pivotal role in regulation of apoptosis and survival in cells. The cellular activities of DAPK are tightly regulated by intracellular calcium levels, an inhibitory autophosphorylation site (S308) within the CaM-binding domain, and by proteasomal degradation. Preliminary studies from this laboratory have suggested that DAPK has a major role in signaling by the inflammatory cytokine, TNF and becomes associated with TNFR1 in response to TNF. To better understand the mechanism by which DAPK regulates apoptotic responses to the cytokine TNF, we have examined the downstream arms of TNFR1 signaling cascade. These studies have revealed that maximal activation of c-Jun N-terminal kinase (JNK) in response to TNF is dependent upon the activities of DAPK. Data shows that upon siRNA mediated depletion of DAPK, JNK 1 activation is significantly attenuated. However, there is no detectable effect on NFkB, p38, or ERK 1/2 activation. This data has identified a novel-signaling pathway for DAPK, in the regulation of survival, inflammation, and proliferation signals through modulation of MAPK/JNK activation. Ongoing studies are focused on elucidating the mechanism of DAPK activation of the MAPK/JNK pathway and the physiological role of this interaction. Supported by HL54118 and DK062810 to PJG
DAPK mediates TNF-alpha induced apoptosis by TNF-receptor 1 association and JNK activation through MKK7 (Meeting Abstract)
The FASEB Journal
Death Associated Protein Kinase (DAPK) is a calcium calmodulin (CaM) regulated serine/threonine kinase, which has a pivotal role in regulation of apoptosis and survival in cells. The cellular activities of DAPK are tightly regulated by intracellular calcium levels, an inhibitory autophosphorylation site (S308) within the CaM-binding domain, and by proteasomal degradation. Preliminary studies from this laboratory have suggested that DAPK has a major role in signaling by the inflammatory cytokine, TNF and becomes associated with TNFR1 in response to TNF. To better understand the mechanism by which DAPK regulates apoptotic responses to the cytokine TNF, we have examined the downstream arms of TNFR1 signaling cascade. These studies have revealed that maximal activation of c-Jun N-terminal kinase (JNK) in response to TNF is dependent upon the activities of DAPK. Data shows that upon siRNA mediated depletion of DAPK, JNK 1 activation is significantly attenuated. However, there is no detectable effect on NFkB, p38, or ERK 1/2 activation. This data has identified a novel-signaling pathway for DAPK, in the regulation of survival, inflammation, and proliferation signals through modulation of MAPK/JNK activation. Ongoing studies are focused on elucidating the mechanism of DAPK activation of the MAPK/JNK pathway and the physiological role of this interaction. Supported by HL54118 and DK062810 to PJG
Mechanisms of Endothelial Dysfunction: Clues from Cyclosporine
Journal of Pharmacology and Toxicology
There has been recent interest in the role of the kidney in the regulation of metabolic byproducts thought to be involved in the induction of endothelial dysfunction. The symptoms include increased blood pressure, decreased kidney function, increase in serum markers such as transforming growth factor beta, reactive oxygen species, asymmetric dimethylated arginine and an increase in the prothrombic and inflammatory state of the vasculature. Pathologies that exhibit this unique set of physiological findings include such diseases as diabetes, hypertension and other types of cardiovascular disease.
DAPK mediates TNF-alpha induced apoptosis by TNF-receptor 1 association and JNK activation through MKK7 (Meeting Abstract)
The FASEB Journal
Death Associated Protein Kinase (DAPK) is a calcium calmodulin (CaM) regulated serine/threonine kinase, which has a pivotal role in regulation of apoptosis and survival in cells. The cellular activities of DAPK are tightly regulated by intracellular calcium levels, an inhibitory autophosphorylation site (S308) within the CaM-binding domain, and by proteasomal degradation. Preliminary studies from this laboratory have suggested that DAPK has a major role in signaling by the inflammatory cytokine, TNF and becomes associated with TNFR1 in response to TNF. To better understand the mechanism by which DAPK regulates apoptotic responses to the cytokine TNF, we have examined the downstream arms of TNFR1 signaling cascade. These studies have revealed that maximal activation of c-Jun N-terminal kinase (JNK) in response to TNF is dependent upon the activities of DAPK. Data shows that upon siRNA mediated depletion of DAPK, JNK 1 activation is significantly attenuated. However, there is no detectable effect on NFkB, p38, or ERK 1/2 activation. This data has identified a novel-signaling pathway for DAPK, in the regulation of survival, inflammation, and proliferation signals through modulation of MAPK/JNK activation. Ongoing studies are focused on elucidating the mechanism of DAPK activation of the MAPK/JNK pathway and the physiological role of this interaction. Supported by HL54118 and DK062810 to PJG
Mechanisms of Endothelial Dysfunction: Clues from Cyclosporine
Journal of Pharmacology and Toxicology
There has been recent interest in the role of the kidney in the regulation of metabolic byproducts thought to be involved in the induction of endothelial dysfunction. The symptoms include increased blood pressure, decreased kidney function, increase in serum markers such as transforming growth factor beta, reactive oxygen species, asymmetric dimethylated arginine and an increase in the prothrombic and inflammatory state of the vasculature. Pathologies that exhibit this unique set of physiological findings include such diseases as diabetes, hypertension and other types of cardiovascular disease.
How Property Tax Caps and Funding Formulas Have Changed the Role of the School Superintendent in Indiana
NCPEA Publications
There has been debate among states as to how to properly fund schools. The debate has been focused on how much funding is supplied through property tax and is motivated by tax payer anger over fluctuating tax bills. Many of the policies have been implemented without looking at the effects that they will have on schools, especially in Indiana, which saw dramatic restructuring of its school funding mechanism and property tax structure. This qualitative study explores the effects of how the current school funding mechanism and property tax caps has changed the job of the school superintendent in Indiana and to elucidate the superintendents' understanding of a general fund referendum, and how the superintendents perceive their role in light of the new financial realities of their school districts.
