James R. Goss
- Cellular and Molecular Neuroscience top 2%
- Molecular Biology top 10%
- Physiology top 5%
- Genetics top 5%
- Epidemiology top 10%
- Co-authors
- Joseph C. GloriosoMarina MataWilliam F. GoinsDavid MorganPatrick M. KochanekSteven T. DeKoskyDarren WolfeDavid J. Fink
- Topics
- Nerve injury and regeneration (18 papers)Pain Mechanisms and Treatments (16 papers)Herpesvirus Infections and Treatments (14 papers)
- Partner nations
- United StatesJapan
In The Last Decade
James R. Goss
56 papers receiving 2.4k citations
Peers
Comparison fields: 5 of 106
- Cellular and Molecular Neuroscience 998
- Molecular Biology 778
- Physiology 622
- Genetics 452
- Epidemiology 449
Countries citing papers authored by James R. Goss
This map shows the geographic impact of James R. Goss's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by James R. Goss with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites James R. Goss more than expected).
Fields of papers citing papers by James R. Goss
This network shows the impact of papers produced by James R. Goss. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by James R. Goss. The network helps show where James R. Goss may publish in the future.
Co-authorship network of co-authors of James R. Goss
This figure shows the co-authorship network connecting the top 25 collaborators of James R. Goss. A scholar is included among the top collaborators of James R. Goss based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with James R. Goss. James R. Goss is excluded from the visualization to improve readability, since they are connected to all nodes in the network.
All Works
| # | Work | Indexed citations |
|---|---|---|
| 1 | 14 | |
| 2 | Inhibition of bladder hypersensitivity by interleukin 4 (IL-4) gene therapy using herpes simplex virus (HSV) vectors in rats with cyclophosphamide induced cystitis | 1 |
| 3 | 16 | |
| 4 | 36 | |
| 5 | 1 | |
| 6 | 44 | |
| 7 | 31 | |
| 8 | 10 | |
| 9 | 85 | |
| 10 | 133 | |
| 11 | 54 | |
| 12 | 69 | |
| 13 | 33 | |
| 14 | 37 | |
| 15 | 82 | |
| 16 | 75 | |
| 17 | 84 | |
| 18 | 138 | |
| 19 | 41 | |
| 20 | 10 |
About James R. Goss
James R. Goss is a scholar working on Cellular and Molecular Neuroscience, Urology and Behavioral Neuroscience, having authored 58 papers that have together received 2.4k indexed citations. Recurring topics across this work include Nerve injury and regeneration (18 papers), Pain Mechanisms and Treatments (16 papers) and Herpesvirus Infections and Treatments (14 papers). The work is most often cited by research in Developmental Neuroscience (263 citations), Cellular and Molecular Neuroscience (998 citations) and Neurology (301 citations). James R. Goss has collaborated with scholars based in United States and Japan. Frequent co-authors include Joseph C. Glorioso, Marina Mata, William F. Goins, David Morgan, Patrick M. Kochanek, Steven T. DeKosky, Darren Wolfe, David J. Fink, Scot Styren and Caleb E. Finch. Their work appears in journals such as Proceedings of the National Academy of Sciences, Gastroenterology and Diabetes.
Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.