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Researcher · IRCCS Eugenio Medea · Italy

S. Gandossini

S. Gandossini publishes mostly in Molecular Biology, Pulmonary and Respiratory Medicine and Cellular and Molecular Neuroscience, on topics such as Muscle Physiology and Disorders, Genetic Neurodegenerative Diseases and Chronic Obstructive Pulmonary Disease (COPD) Research.

ORCID 0000-0002-5340-3458 OpenAlex
World rank
#2,412,622
of 7,710,434 ranked researchers
Rank in Italy
#80,827
of 242,206
Works
50
Citations
1.2k
Citations per work
24.9
h-index
17
i10-index 20Top 42% in Molecular Biology
S. Gandossini

What does S. Gandossini research?

S. Gandossini's work is mostly in Medicine (29%), Biochemistry, Genetics and Molecular Biology (23%), Neuroscience (10%).

Life Sciences: 17 works · 33.1% of their workBiochemistry, Genetics and Molecular Biology: 12 works · 23.4% of their workMolecular Biology: 12 works · 23.4% of their workNeuroscience: 5 works · 9.7% of their workCellular and Molecular Neuroscience: 5 works · 9.7% of their workEverything else: 15 works · 30.5% of their workHealth Sciences: 15 works · 29.1% of their workMedicine: 15 works · 29.1% of their workPulmonary and Respiratory Medicine: 8 works · 15.3% of their workGenetics: 4 works · 7.3% of their workCardiology and Cardiovascular Medicine: 3 works · 6.5% of their workPhysical Sciences: 4 works · 7.3% of their workEngineering: 4 works · 7.3% of their workBiomedical Engineering: 4 works · 7.3% of their workTHEIR WORKS. Gandossini50works
Life Sciences33%Physical Sciences7%Health Sciences29%

Their six largest subfields, inside their fields and domains; the grey slice is everything else they publish. The interactive view splits every one of their works down to single topics.

The fields and subfields, with their numbers
    1. Biochemistry, Genetics and Molecular Biology1223.4%
    2. Neuroscience59.7%
  2. Everything else1530.5%
    1. Medicine1529.1%
    1. Engineering47.3%
  1. 1Molecular Biology23% of their works
  2. 2Pulmonary and Respiratory Medicine15% of their works
  3. 3Cellular and Molecular Neuroscience10% of their works
  4. 4Genetics7% of their works
  5. 5Biomedical Engineering7% of their works
  6. 6Cardiology and Cardiovascular Medicine6% of their works

Research topics

Which keywords describe S. Gandossini's research?

The keywords of their largest research topics: Muscle Regeneration, Skeletal Muscle Atrophy, Mitochondrial Dysfunction, Huntington's Disease, Protein Aggregation, COPD, spirometry and Acute Lung Injury.

Size is their works in the topics tagged with each word, from their 8 largest topics. Each links to the topic it comes from most. The words come from the keyword list OpenAlex gives each topic, not from the text of the papers, so a word can appear that none of the papers uses.

All 18 words, with their numbers
  1. Muscle Regeneration221 topic
  2. Skeletal Muscle Atrophy221 topic
  3. Mitochondrial Dysfunction183 topics
  4. Huntington's Disease111 topic
  5. Protein Aggregation111 topic
  6. COPD91 topic
  7. spirometry91 topic
  8. Acute Lung Injury81 topic
  9. Mechanical Ventilation81 topic
  10. Metabolic Regulation72 topics
  11. SMN171 topic
  12. Spinal Muscular Atrophy71 topic
  13. Cardiomyopathies51 topic
  14. Genetic Mutations51 topic
  15. Brown Adipose Tissue41 topic
  16. Thermogenesis41 topic
  17. Mitochondria31 topic
  18. Reactive Oxygen Species31 topic

Where does S. Gandossini work?

S. Gandossini's main affiliation in the publication record is IRCCS Eugenio Medea, Italy.

How many publications and citations does S. Gandossini have?

OpenAlex counts 50 works and 1,246 citations for S. Gandossini, an h-index of 17, ranking #2,412,622 of 7,710,434 researchers worldwide on the quality score.

Ranked on field-normalised citation excellence (50%), output (30%) and citations (20%). Counts come from OpenAlex author records, which occasionally merge different people who share a name or split one person into several.

Papers, co-authors, who cited this work and researchers on the nearest topics have tabs of their own, above. Is this your page? Claim it with your ORCID iD, or request a correction or removal.

Discussion

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