The Wall of Scholarship acknowledges current UI Carver College of Medicine faculty who are first or senior authors of published research articles that have made a significant impact on a particular field of science or medicine.
Specifically, the research papers have been cited more than 1,000 times in subsequent published research articles, based on at least two of three recognized academic citation indices: Google Scholar, Scopus, and Web of Science.
The following faculty achieved Wall of Scholarship distinction during the 2021 calendar year:
Ted Abel, PhD
Professor and chair, Department of Neuroscience and Pharmacology
Director, Iowa Neuroscience Institute
Co-Director, Hawkeye Intellectual and Developmental Disabilities Research Center
Roy J. Carver Chair in Neuroscience
Genetic Demonstration of a Role for PKA in the Late Phase of LTP and in Hippocampus-Based Long-Term Memory
Cell. 1997 Mar 7;88(5):615-626
Abel’s paper is based on work that was carried out while he was a Damon Runyon/Walter Winchell postdoctoral fellow with Eric Kandel, MD, in the Howard Hughes Medical Institute and Columbia University College of Physicians & Surgeons.
The experiments described in this paper were the first to link a specific form of synaptic plasticity and a specific molecular mechanism to long-term memory—supporting the idea that memory is stored in the strength of neuronal connections.
This paper was a critical component of research that led to Kandel receiving the Nobel Prize in Physiology or Medicine in 2000.
Robert Mullins, PhD
Professor, Department of Ophthalmology and Visual Sciences
Martin Carver Chair in Ocular Cell Biology
An Integrated Hypothesis That Considers Drusen as Biomarkers of Immune-Mediated Processes at the RPE-Bruch’s Membrane Interface in Aging and Age-Related Macular Degeneration
Progress in Retinal and Eye Research. 2001;20(6):705-732
Age-related macular degeneration is a major cause of blindness—one that affects millions of people in the United States. The cellular and molecular events that contribute to AMD have been largely unknown.
In this manuscript by Mullins and colleagues, new and previously unpublished data were synthesized in order to understand the composition and origin of drusen, which are yellow deposits under the retina that are characteristic of AMD.
Stanley Perlman, MD, PhD
Professor, Department of Microbiology and Immunology
Pathogenic Human Coronavirus Infections: Causes and Consequences of Cytokine Storm and Immunopathology
Seminars in Immunopathology. 2017 Jul;39:529-539.
There is a balance in any infection between the infectious agent and the host response to the pathogen. Perlman’s review describes this relationship in the context of coronavirus infections.
Well before the COVID-19 pandemic began, it was known that infected animals had trouble eliminating coronaviruses without causing damage to tissues in the infected host.
This paper described the understanding of these interactions prior to the pandemic. The information became important and timely when it was realized that similar mechanisms were present in humans infected with SARS-CoV-2. As a result, this review was cited extensively as people tried to grapple with understanding the basis of disease in COVID-19.
Coronaviruses Post-SARS: An Overview of their Replication and Pathogenesis
Methods in Molecular Biology. 2015;1282:1-23
In the earliest days of the COVID-19 pandemic, coronaviruses were studied by only a few laboratories. This review summarized the state of knowledge of these viruses—covering both the biology of the virus and the pathogenesis of the diseases caused by this family of viruses.
As a result, this article was read and cited by many new contributors to the coronavirus field, as well as others wanting to learn more about coronaviruses.
Michael Welsh, MD
Professor, Department of Internal Medicine–Pulmonary, Critical Care, and Occupational Medicine
Director, Pappajohn Biomedical Institute
Investigator, Howard Hughes Medical Institute
Processing of Mutant Cystic Fibrosis Transmembrane Conductance Regulator is Temperature-Sensitive
Nature. 1992 Aug 27;358:761-764
Mutations in the CFTR gene cause cystic fibrosis, which is a lethal genetic disease. In earlier work, Welsh and his colleagues discovered what CFTR does: It is a channel that allows salt chloride to move across cell membranes. Their research had also revealed how mutations disrupt CFTR, preventing it from working appropriately.
In this paper, Welsh and colleagues discovered that reducing the temperature of cells restores function to CFTR with the most common mutation and initiates chloride movement.
The demonstration that it was possible to repair the common CFTR defect ignited efforts to develop a drug that could have the same effect in repairing mutant CFTR. Today, the lives of people with cystic fibrosis are dramatically improved by medicines that resulted from this research.