Research Meetings
December 2017 through January 2018


December 11, 2017 ( Monday )

12:00pm - 1:00pm
Department of Biology Donut Talk

Dr. J. C. Price, Brigham Young University

"Investigating dynamics of ribosome structure and activity"


Location:  Hutchison Hall, Lander Auditorium

Posted by:  Deborah Lawrence, Biology, 30-Aug-17 11:46am ET


December 14, 2017 ( Thursday )

10:00am
PhD Thesis Defense

Mary Grantham, University of Rochester

"The Molecular Basis of the Pea Aphid Wing Polyphenism"

Location:  Hutchison 473

Posted by:  Brenna Rybak, Biology, 20-Nov-17 8:56am ET


12:30pm - 1:30pm
Department of Pharmacology and Physiology Colloquium Series - Research Seminar

TITLE: TBA



Speaker: Si (Vivian) Chen

Graduate Student in the laboratory of Dr. Chen Yan



Location: Medical Center, Room 4-6912



For more information, contact Erica Fedigan.

Location:  Medical Center, Anders Room (4-6912)

Posted by:  Erica Fedigan, Pharmacology, 28-Aug-17 2:10pm ET


December 21, 2017 ( Thursday )

12:30pm - 1:30pm
Department of Pharmacology and Physiology Colloquium Series - Research Seminar

TITLE: TBA



Speaker: Emma W. Grygotis

Graduate Student in the laboratory of Dr. Denise C. Hocking



Location: Medical Center, Room 4-6912



For more information, contact Erica Fedigan.

Location:  Medical Center, Anders Room (4-6912)

Posted by:  Erica Fedigan, Pharmacology, 28-Aug-17 2:11pm ET


January 9, 2018 ( Tuesday )

4:00pm - 5:00pm
THE Aab CVRI Seminar Series

Location:  CVRI Conf. Room # G.11211/G.11213 MRBX/Delmonte Bldg - (Ground floor)

Posted by:  Jacqueline Velazquez, Cardiovascular Research Institute, 9-Jan-17 2:03pm ET


January 10, 2018 ( Wednesday )

12:30pm - 1:30pm
Center for Oral Biology Bagel Talk Series 2018

Catherine Ovitt, Ph.D.

Associate Professor of Biomedical Genetics in the Center for Oral Biology

"Bubbles, chips and spheres: Engineering a salivary gland tissue chip"


Location:  COB Conference room, G9654, KMRB

Posted by:  Nicole Beaumont, Center for Oral Biology, 6-Dec-17 11:14am ET


January 18, 2018 ( Thursday )

4:00pm - 5:00pm
The Aab CVRI Seminar Series

SPEAKER: Kirk M. McHugh, Ph.D. Professor & Director Division of Anatomy Department of Biomedical Education & Anatomy The Ohio State University

Professor & Directors Nephrology & Urology Research Affinity Center for Biomedical and Translational Research Nationwide Children's Hospital

TITLE OF TALK: "Megabladder Mouse Model of Abnormal Detrusor and Cardiac Outflow Tract Smooth Muscle Development"

Research Summary: My research efforts focus on the normal development and pathogenesis of the urogenital system. Urinary tract malformations, obstructive nephropathy, and renal hypoplasia/dysplasia comprise over 50% of the children with end-stage renal disease worldwide. These defects are extremely important in the terms of health care costs, with end-stage renal disease costing 1.5 billion dollars annually. Studies in my lab focus on congenital defects in bladder development and the resulting sequelae associated with obstructive nephropathy and chronic kidney disease (CKD). We have identified a highly unique mouse model known as the megabladder (mgb) that represents the first animal model of congenital obstructive nephropathy. We use a wide range of genetic and molecular approaches to study the pathogenic changes in mgb-/- renal function that are associated with the development of chronic kidney disease (CKD) and end stage renal disease (ESRD). These studies have lead to a novel renal adaptation model that involves the integrated balance between TGF-mediated pathogenesis, retinoic acid mediated remodeling/repair and steroid hormone modulation. Genetic studies of the mgb-/- mouse mutation indicate that these animals possess a complex deletion/translocation defect associated with chromosomes 16 and 11. The deletion/translocation site on chromosome 11 occurs 1+ Mb upstream of the myocardin gene and appears to have disrupted a long-range, tissue-specific enhancer element that is responsible for up-regulation of myocardin expression in the bladder. These genetic defects result in the production of a hypomorphic allele that reduces myocardin expression in the bladder by 75%. Further reduction in myocardin expression to 90% results in the appearance of a second defect, patent ductus arteriosus, that results in early postnatal lethality in these animals.

Location:  CVRI Conf. Room # G.11211/G.11213 MRBX/Delmonte Bldg - (Ground floor)

Posted by:  Jacqueline Velazquez, Cardiovascular Research Institute, 9-Jan-17 1:52pm ET


4:00pm - 5:00pm
THE Aab CVRI Seminar Series

SPEAKER: Kirk M. McHugh, Ph.D. Professor & Director Division of Anatomy Department of Biomedical Education & Anatomy The Ohio State University

Professor & Directors Nephrology & Urology Research Affinity Center for Biomedical and Translational Research Nationwide Children's Hospital

TITLE OF TALK: "Megabladder Mouse Model of Abnormal Detrusor and Cardiac Outflow Tract Smooth Muscle Development"

Research Summary: My research efforts focus on the normal development and pathogenesis of the urogenital system. Urinary tract malformations, obstructive nephropathy, and renal hypoplasia/dysplasia comprise over 50% of the children with end-stage renal disease worldwide. These defects are extremely important in the terms of health care costs, with end-stage renal disease costing 1.5 billion dollars annually. Studies in my lab focus on congenital defects in bladder development and the resulting sequelae associated with obstructive nephropathy and chronic kidney disease (CKD). We have identified a highly unique mouse model known as the megabladder (mgb) that represents the first animal model of congenital obstructive nephropathy. We use a wide range of genetic and molecular approaches to study the pathogenic changes in mgb-/- renal function that are associated with the development of chronic kidney disease (CKD) and end stage renal disease (ESRD). These studies have lead to a novel renal adaptation model that involves the integrated balance between TGF-mediated pathogenesis, retinoic acid mediated remodeling/repair and steroid hormone modulation. Genetic studies of the mgb-/- mouse mutation indicate that these animals possess a complex deletion/translocation defect associated with chromosomes 16 and 11. The deletion/translocation site on chromosome 11 occurs 1+ Mb upstream of the myocardin gene and appears to have disrupted a long-range, tissue-specific enhancer element that is responsible for up-regulation of myocardin expression in the bladder. These genetic defects result in the production of a hypomorphic allele that reduces myocardin expression in the bladder by 75%. Further reduction in myocardin expression to 90% results in the appearance of a second defect, patent ductus arteriosus, that results in early postnatal lethality in these animals.

Location:  CVRI Conf. Room # G.11211/G.11213 MRBX/Delmonte Bldg - (Ground floor)

Posted by:  Jacqueline Velazquez, Cardiovascular Research Institute, 9-Jan-17 1:53pm ET


4:00pm - 5:00pm
THE Aab CVRI Seminar Series

SPEAKER: Kirk M. McHugh, Ph.D. Professor & Director Division of Anatomy Department of Biomedical Education & Anatomy The Ohio State University

Professor & Directors Nephrology & Urology Research Affinity Center for Biomedical and Translational Research Nationwide Children's Hospital

TITLE OF TALK: "Megabladder Mouse Model of Abnormal Detrusor and Cardiac Outflow Tract Smooth Muscle Development"

Research Summary: My research efforts focus on the normal development and pathogenesis of the urogenital system. Urinary tract malformations, obstructive nephropathy, and renal hypoplasia/dysplasia comprise over 50% of the children with end-stage renal disease worldwide. These defects are extremely important in the terms of health care costs, with end-stage renal disease costing 1.5 billion dollars annually. Studies in my lab focus on congenital defects in bladder development and the resulting sequelae associated with obstructive nephropathy and chronic kidney disease (CKD). We have identified a highly unique mouse model known as the megabladder (mgb) that represents the first animal model of congenital obstructive nephropathy. We use a wide range of genetic and molecular approaches to study the pathogenic changes in mgb-/- renal function that are associated with the development of chronic kidney disease (CKD) and end stage renal disease (ESRD). These studies have lead to a novel renal adaptation model that involves the integrated balance between TGF-mediated pathogenesis, retinoic acid mediated remodeling/repair and steroid hormone modulation. Genetic studies of the mgb-/- mouse mutation indicate that these animals possess a complex deletion/translocation defect associated with chromosomes 16 and 11. The deletion/translocation site on chromosome 11 occurs 1+ Mb upstream of the myocardin gene and appears to have disrupted a long-range, tissue-specific enhancer element that is responsible for up-regulation of myocardin expression in the bladder. These genetic defects result in the production of a hypomorphic allele that reduces myocardin expression in the bladder by 75%. Further reduction in myocardin expression to 90% results in the appearance of a second defect, patent ductus arteriosus, that results in early postnatal lethality in these animals.

Location:  CVRI Conf. Room # G.11211/G.11213 MRBX/Delmonte Bldg - (Ground floor)

Posted by:  Jacqueline Velazquez, Cardiovascular Research Institute, 9-Jan-17 2:01pm ET