Lawrence Z. Stern
- Molecular Biology top 10%
- Cellular and Molecular Neuroscience top 5%
- Neurology top 5%
- Physiology top 10%
- Pharmacology top 5%
- Co-authors
- Henry I. YamamuraGregory J. WastekRaphael GruenerS.J. EnnaReuven SandykClaire M. PayneJames AllenderPaul Consroe
- Topics
- Muscle Physiology and Disorders (23 papers)Genetic Neurodegenerative Diseases (13 papers)Ion channel regulation and function (10 papers)
- Partner nations
- United StatesUnited KingdomSweden
In The Last Decade
Lawrence Z. Stern
70 papers receiving 1.7k citations
Peers
Comparison fields: 5 of 114
- Molecular Biology 719
- Cellular and Molecular Neuroscience 612
- Neurology 280
- Physiology 277
- Pharmacology 255
Countries citing papers authored by Lawrence Z. Stern
This map shows the geographic impact of Lawrence Z. Stern'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 Lawrence Z. Stern with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Lawrence Z. Stern more than expected).
Fields of papers citing papers by Lawrence Z. Stern
This network shows the impact of papers produced by Lawrence Z. Stern. 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 Lawrence Z. Stern. The network helps show where Lawrence Z. Stern may publish in the future.
Co-authorship network of co-authors of Lawrence Z. Stern
This figure shows the co-authorship network connecting the top 25 collaborators of Lawrence Z. Stern. A scholar is included among the top collaborators of Lawrence Z. Stern 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 Lawrence Z. Stern. Lawrence Z. Stern is excluded from the visualization to improve readability, since they are connected to all nodes in the network.
All Works
| # | Work | Indexed citations |
|---|---|---|
| 1 | 49 | |
| 2 | 253 | |
| 3 | 2 | |
| 4 | 6 | |
| 5 | 39 | |
| 6 | 6 | |
| 7 | 51 | |
| 8 | Changes in end-plate cholinesterase and axons during muscle degeneration and regeneration. | 14 |
| 9 | 71 | |
| 10 | 13 | |
| 11 | 1 | |
| 12 | 13 | |
| 13 | 8 | |
| 14 | 12 | |
| 15 | 4 | |
| 16 | 125 | |
| 17 | 44 | |
| 18 | 6 | |
| 19 | 25 | |
| 20 | 18 |
About Lawrence Z. Stern
Lawrence Z. Stern is a scholar working on Cellular and Molecular Neuroscience, Neurology and Molecular Biology, having authored 70 papers that have together received 1.9k indexed citations. Recurring topics across this work include Muscle Physiology and Disorders (23 papers), Genetic Neurodegenerative Diseases (13 papers) and Ion channel regulation and function (10 papers). The work is most often cited by research in Cellular and Molecular Neuroscience (612 citations), Neurology (280 citations) and Pharmacology (255 citations). Lawrence Z. Stern has collaborated with scholars based in United States, United Kingdom and Sweden. Frequent co-authors include Henry I. Yamamura, Gregory J. Wastek, Raphael Gruener, S.J. Enna, Reuven Sandyk, Claire M. Payne, James Allender, Paul Consroe, Karl H. Schram and Stuart R. Snider. Their work appears in journals such as JAMA, Circulation and Journal of the American College of Cardiology.
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.