F. Ichikawa
Impact in
-
- Diabetes Management and Research
- Diet, Metabolism, and Disease
- Physiology top 10%
- Adipose Tissue and Metabolism
- Diet and metabolism studies
Papers in
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- Metabolism, Diabetes, and Cancer 3
- Receptor Mechanisms and Signaling 3
- Surgery 5
- Pancreatic function and diabetes 5
- Co-authors
- Xiaohong Yuan (9 shared papers)Kentaro Yamada (9 shared papers)K. Nonaka (6 shared papers)S. Ishiyama‐Shigemoto (4 shared papers)Wasaku Koyama (4 shared papers)K. Koyama (4 shared papers)Kyohei Nonaka (4 shared papers)Xiaohong Yuan (1 shared paper)
- Journals
- Diabetologia (4 papers)Diabetes Research and Clinical Practice (2 papers)The Journal of Clinical Endocrinology & Metabolism (1 paper)Diabetes Care (1 paper)Diabetes (1 paper)
- Partner nations
- JapanUnited States
In The Last Decade
F. Ichikawa
11 papers receiving 631 citations
Peers
Comparison fields: 5 of 64
- Endocrinology, Diabetes and Metabolism 164
- Physiology 203
- Genetics 198
- Endocrine and Autonomic Systems 44
- Surgery 201
Countries citing papers authored by F. Ichikawa
This map shows the geographic impact of F. Ichikawa'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 F. Ichikawa with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites F. Ichikawa more than expected).
Fields of papers citing papers by F. Ichikawa
This network shows the impact of papers produced by F. Ichikawa. 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 F. Ichikawa. The network helps show where F. Ichikawa may publish in the future.
Co-authors
The 17 scholars most cited alongside F. Ichikawa, linked wherever they have co-authored with each other. Click a name or a connecting line to browse the papers they share.
All Works
| # | Work | ||
|---|---|---|---|
| 1 | 1996 | 168 | |
| 2 | 1999 | 141 | |
| 3 | 1997 | 101 | |
| 4 | 1999 | 63 | |
| 5 | 1999 | 47 | |
| 6 | 1999 | 46 | |
| 7 | 1997 | 25 | |
| 8 | 1997 | 19 | |
| 9 | 1997 | 16 | |
| 10 | 1998 | 10 | |
| 11 | 1995 | 4 |
About F. Ichikawa
F. Ichikawa is a scholar working on Molecular Biology, Surgery, Genetics, Physiology and Immunology, having authored 11 papers that have together received 640 indexed citations. Recurring topics across this work include Pancreatic function and diabetes (5 papers), Diabetes and associated disorders (4 papers), Metabolism, Diabetes, and Cancer (3 papers), Adipose Tissue and Metabolism (3 papers), Receptor Mechanisms and Signaling (3 papers), Diet and metabolism studies (2 papers), Neonatal Health and Biochemistry (1 paper) and Phagocytosis and Immune Regulation (1 paper). The work is most often cited by research in Endocrinology, Diabetes and Metabolism (164 citations), Physiology (203 citations), Genetics (198 citations), Endocrine and Autonomic Systems (44 citations) and Surgery (201 citations). F. Ichikawa has collaborated with scholars based in Japan and United States. Frequent co-authors include Xiaohong Yuan, Kentaro Yamada, K. Nonaka, S. Ishiyama‐Shigemoto, Wasaku Koyama, K. Koyama, Kyohei Nonaka, Xiaohong Yuan, Hideki Hayashi and Shingo Shoji. Their work appears in journals such as Diabetologia, Diabetes Research and Clinical Practice, The Journal of Clinical Endocrinology & Metabolism, Diabetes Care 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.