Ian McFadzean
- Molecular Biology top 10%
- Cellular and Molecular Neuroscience top 5%
- Physiology top 10%
- Sensory Systems top 1%
- Cardiology and Cardiovascular Medicine top 10%
- Co-authors
- Alan GibsonC. WaymanA GibsonP WallaceR. J. DochertyDavid A. BrownJohn F. TuckerGraeme Milligan
- Topics
- Ion channel regulation and function (19 papers)Pain Mechanisms and Treatments (14 papers)Ion Channels and Receptors (9 papers)
- Partner nations
- United KingdomUnited StatesSwitzerland
In The Last Decade
Ian McFadzean
32 papers receiving 1.2k citations
Peers
Comparison fields: 5 of 94
- Molecular Biology 845
- Cellular and Molecular Neuroscience 532
- Physiology 346
- Sensory Systems 306
- Cardiology and Cardiovascular Medicine 156
Countries citing papers authored by Ian McFadzean
This map shows the geographic impact of Ian McFadzean'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 Ian McFadzean with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Ian McFadzean more than expected).
Fields of papers citing papers by Ian McFadzean
This network shows the impact of papers produced by Ian McFadzean. 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 Ian McFadzean. The network helps show where Ian McFadzean may publish in the future.
Co-authorship network of co-authors of Ian McFadzean
This figure shows the co-authorship network connecting the top 25 collaborators of Ian McFadzean. A scholar is included among the top collaborators of Ian McFadzean 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 Ian McFadzean. Ian McFadzean is excluded from the visualization to improve readability, since they are connected to all nodes in the network.
All Works
| # | Work | Indexed citations |
|---|---|---|
| 1 | 3 | |
| 2 | 44 | |
| 3 | 2 | |
| 4 | 25 | |
| 5 | The Rho kinase inhibitor, Y-27632, inhibits contractile responses to carbachol, thapsigargin and potassium in the mouse anococcygeus | 1 |
| 6 | 219 | |
| 7 | 23 | |
| 8 | 27 | |
| 9 | 40 | |
| 10 | 30 | |
| 11 | 81 | |
| 12 | 6 | |
| 13 | 6 | |
| 14 | 37 | |
| 15 | 3 | |
| 16 | 14 | |
| 17 | 134 | |
| 18 | 30 | |
| 19 | 29 | |
| 20 | 81 |
About Ian McFadzean
Ian McFadzean is a scholar working on Sensory Systems, Cellular and Molecular Neuroscience and Physiology, having authored 32 papers that have together received 1.2k indexed citations. Recurring topics across this work include Ion channel regulation and function (19 papers), Pain Mechanisms and Treatments (14 papers) and Ion Channels and Receptors (9 papers). The work is most often cited by research in Sensory Systems (306 citations), Cellular and Molecular Neuroscience (532 citations) and Physiology (346 citations). Ian McFadzean has collaborated with scholars based in United Kingdom, United States and Switzerland. Frequent co-authors include Alan Gibson, C. Wayman, A Gibson, P Wallace, R. J. Docherty, David A. Brown, John F. Tucker, Graeme Milligan, Ian Mullaney and R.G. Hill. Their work appears in journals such as Neuron, Circulation Research and Biochemical and Biophysical Research Communications.
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.