philipp malsch: h-index, Total Citations, and Citation Map
philipp malsch's h-index is 7 (7 i10-index, 246+ total citations across 5+ publications) according to Google Scholar as of May 2026. philipp malsch is affiliated with Unknown affiliation.
philipp malsch is a researcher affiliated with Unknown affiliation, specializing in various fields. Their work has been cited 246 times. This profile visualizes their global influence, highlighting strong citation networks in Austria.
philipp malsch's Citation Metrics
Bibliometric impact based on 5 indexed publications.
- H-Index
- 7
- i10-Index
- 7
- Total Citations
- 246
- Citing Countries
- 11
As of May 2026.
philipp malsch has an h-index of 7 and 246 total citations across 5 publications, with research cited by institutions in 11 countries.
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Top Cited Works
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Deletion of interleukin-6 signal transducer gp130 in small sensory neurons attenuates mechanonociception and down-regulates TRPA1 expression
201497
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Visa Evidence Package
Views and exports tuned for EB-1A, O-1A, and EB-2 NIW petitions. Sustained acclaim, geographic reach, and independent-citation filtering are the strongest evidence categories immigration adjudicators look for.
Significant Contributions
Auto-detected research lines — a seminal paper and the follow-up work building on it. Review and edit before using in a petition. Each Free PDF opens in a new tab — EB-1A organises this into the structure USCIS applies to Criterion 5 of 8 CFR § 204.5(h)(3)(v); EB-1B re-frames it under § 204.5(i)(3) (outstanding researcher); NIW presents it under prong 2 of Matter of Dhanasar.
The researcher elucidated the role of gp130 signaling in small sensory neurons, demonstrating its critical function in mechanonociception and TRPA1 expression regulation.
The researcher elucidated the molecular mechanism linking gp130 deficiency to reduced nociceptor excitability via Kcna4 channel upregulation and increased potassium currents.
The researcher advanced the understanding of multiple system atrophy by demonstrating peripheral nerve involvement in the transgenic PLP-α-Syn model, thereby extending the disease phenotype.
Citation trend (last 10 years)Click to expand
Citation Trend (Last 10 Years)
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