Automated Author ProfileTorabian, Panteha
Torabian, Panteha
Current S-Index
Sum of Dataset Indices for all datasets
Average Dataset Index per Dataset
Average Dataset Index per dataset
Total Datasets
Total datasets for this author
Average FAIR Score
Average FAIR Score per dataset
Total Citations
Total citations to the author's datasets
Total Mentions
Total mentions of the author's datasets
S-Index Interpretation
The S-Index (Sharing Index) is a comprehensive metric that represents the cumulative impact of all your datasets. It is calculated as the sum of Dataset Index scores across all your claimed datasets.
What it means:
- A higher S-index indicates greater overall impact of your datasets relative to typical datasets in their fields of research
- The S-Index grows as you add more datasets or as existing datasets gain more citations and mentions
- It provides a single number to track your research data impact over time
Current S-Index: 1.2 (sum of 6 datasets Dataset Index scores)
More information here.
S-Index Over Time
Cumulative Citations Over Time
Cumulative Mentions Over Time
Datasets
Fluorescence data, NTA data, western blot data, LPS quantification data, permeability data, and cytokine concentration data
Authors
- Widom, Louis ;
- Torabian, Panteha ;
- Trempel, Michelle ;
- McCloskey, Molly ;
- Michel, Lea ;
- McGrath, James L. ;
- Gaborski, Thomas R.
Fluorescence data, NTA data, western blot data, LPS quantification data, permeability data, and cytokine concentration data
Authors
- Widom, Louis ;
- Torabian, Panteha ;
- Trempel, Michelle ;
- McCloskey, Molly ;
- Michel, Lea ;
- McGrath, James L. ;
- Gaborski, Thomas R.
Antibiotic treatment is essential for resolving bacterial infections, but its impact on bacterial extracellular vesicle (BEV) production and downstream host responses remains underexplored. We studied how three common antibiotics affect BEV release and inflammatory signaling from two strains of Escherichia coli associated with urinary tract infections and meningitis. We found that BEVs from both strains activated human endothelial cells through toll-like receptor 4, and that this response was modulated by antibiotic use. In particular, meropenem altered both BEV production and pro-inflammatory potential in a strain-dependent manner. Proteomic analysis revealed that antibiotic exposure modified BEV protein content, including levels of the immunogenic lipoprotein Lpp. These results suggest that antibiotic choice can influence bacterial signaling to the host via vesicles in a strain-dependent manner. Understanding how antibiotics reshape vesicle-mediated communication may offer new insights into sepsis and endothelial dysfunction.These TSV files contain mass spectrometry data from BEVs derived from E. coli strain CFT073 [WAM2267] following exposure to antibiotics meropenem (Mero), tobramycin (Tobra), ciprofloxacin (Cipro), or no antibiotics (Ctrl)
Authors
- Widom, Louis ;
- Torabian, Panteha ;
- Wojehowski, Abigail ;
- Ghaemmaghami, Sina ;
- Michel, Lea V. ;
- Gaborski, Thomas R.
Antibiotic treatment is essential for resolving bacterial infections, but its impact on bacterial extracellular vesicle (BEV) production and downstream host responses remains underexplored. We studied how three common antibiotics affect BEV release and inflammatory signaling from two strains of Escherichia coli associated with urinary tract infections and meningitis. We found that BEVs from both strains activated human endothelial cells through toll-like receptor 4, and that this response was modulated by antibiotic use. In particular, meropenem altered both BEV production and pro-inflammatory potential in a strain-dependent manner. Proteomic analysis revealed that antibiotic exposure modified BEV protein content, including levels of the immunogenic lipoprotein Lpp. These results suggest that antibiotic choice can influence bacterial signaling to the host via vesicles in a strain-dependent manner. Understanding how antibiotics reshape vesicle-mediated communication may offer new insights into sepsis and endothelial dysfunction.These TSV files contain mass spectrometry data from BEVs derived from E. coli strain CFT073 [WAM2267] following exposure to antibiotics meropenem (Mero), tobramycin (Tobra), ciprofloxacin (Cipro), or no antibiotics (Ctrl)
Authors
- Widom, Louis ;
- Torabian, Panteha ;
- Wojehowski, Abigail ;
- Ghaemmaghami, Sina ;
- Michel, Lea V. ;
- Gaborski, Thomas R.
Antibiotic treatment is essential for resolving bacterial infections, but its impact on bacterial extracellular vesicle (BEV) production and downstream host responses remains underexplored. We studied how three common antibiotics affect BEV release and inflammatory signaling from two strains of Escherichia coli associated with urinary tract infections and meningitis. We found that BEVs from both strains activated human endothelial cells through toll-like receptor 4, and that this response was modulated by antibiotic use. In particular, meropenem altered both BEV production and pro-inflammatory potential in a strain-dependent manner. Proteomic analysis revealed that antibiotic exposure modified BEV protein content, including levels of the immunogenic lipoprotein Lpp. These results suggest that antibiotic choice can influence bacterial signaling to the host via vesicles in a strain-dependent manner. Understanding how antibiotics reshape vesicle-mediated communication may offer new insights into sepsis and endothelial dysfunction.
This Excel file contains the ICAM-1 fluorescence intensity measurements, nanoparticle tracking analysis concentrations and particle sizes, and Western Blot analysis.
Authors
- Widom, Louis ;
- Torabian, Panteha ;
- Wojehowski, Abigail ;
- Ghaemmaghami, Sina ;
- Michel, Lea V. ;
- Gaborski, Thomas R.
Antibiotic treatment is essential for resolving bacterial infections, but its impact on bacterial extracellular vesicle (BEV) production and downstream host responses remains underexplored. We studied how three common antibiotics affect BEV release and inflammatory signaling from two strains of Escherichia coli associated with urinary tract infections and meningitis. We found that BEVs from both strains activated human endothelial cells through toll-like receptor 4, and that this response was modulated by antibiotic use. In particular, meropenem altered both BEV production and pro-inflammatory potential in a strain-dependent manner. Proteomic analysis revealed that antibiotic exposure modified BEV protein content, including levels of the immunogenic lipoprotein Lpp. These results suggest that antibiotic choice can influence bacterial signaling to the host via vesicles in a strain-dependent manner. Understanding how antibiotics reshape vesicle-mediated communication may offer new insights into sepsis and endothelial dysfunction.
This Excel file contains the ICAM-1 fluorescence intensity measurements, nanoparticle tracking analysis concentrations and particle sizes, and Western Blot analysis.
Authors
- Widom, Louis ;
- Torabian, Panteha ;
- Wojehowski, Abigail ;
- Ghaemmaghami, Sina ;
- Michel, Lea V. ;
- Gaborski, Thomas R.