Automated Organization ProfileDepartment of Ophthalmology, Tohoku University Graduate School of Medicine, Japan
Department of Ophthalmology, Tohoku University Graduate School of Medicine, Japan
Current S-Index
Sum of Dataset Indices for all datasets
Average Dataset Index per Dataset
Average Dataset Index per dataset
Total Datasets
Total datasets in this organization
Average FAIR Score
Average FAIR Score per dataset
Total Citations
Total citations to the organization's datasets
Total Mentions
Total mentions of the organization'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: 7.4 (sum of 4 datasets Dataset Index scores)
More information here.
S-Index Over Time
Cumulative Citations Over Time
Cumulative Mentions Over Time
Datasets
This dataset supports the findings of the manuscript titled:"Involvement of microglia in retinal ganglion cell injury induced by IOP elevation in a rat ex vivo acute glaucoma model."In this study, we used a rat ex vivo model of acute intraocular pressure (IOP) elevation to investigate the role of microglia in retinal ganglion cell (RGC) injury. Our results demonstrate that pressure-induced activation of the TLR4-NLRP3 inflammasome cascade contributes to microglial proliferation and IL-1β production, leading to RGC apoptosis. Pharmacological depletion of microglia using the CSF-1R inhibitor PLX5622 suppressed this inflammatory pathway and preserved RGCs.The uploaded files include:- Raw and normalized data from flat-mounted immunostaining (RGC and microglia counts), Western blot membranes (protein expression), TUNEL-stained cryosections (apoptosis), and Epon-embedded sections (NFL thickness and NDS evaluation).- Source data used to generate the figures.This dataset is made available to promote transparency and reproducibility in glaucoma research, particularly in studies involving retinal neuroinflammation and microglial modulation.
Authors
- Sato, Taimu ;
- Ishikawa, Makoto ;
- Izumi, Yukitoshi ;
- Shibata, Naoya ;
- Kota, Sato ;
- Ohno-Oishi, Michiko ;
- Tawarayama, Hiroshi ;
- Kunikata, Hiroshi ;
- Zorumski, Charles F. ;
- Nakawaza, Toru
This dataset supports the findings of the manuscript titled:"Involvement of microglia in retinal ganglion cell injury induced by IOP elevation in a rat ex vivo acute glaucoma model."In this study, we used a rat ex vivo model of acute intraocular pressure (IOP) elevation to investigate the role of microglia in retinal ganglion cell (RGC) injury. Our results demonstrate that pressure-induced activation of the TLR4-NLRP3 inflammasome cascade contributes to microglial proliferation and IL-1β production, leading to RGC apoptosis. Pharmacological depletion of microglia using the CSF-1R inhibitor PLX5622 suppressed this inflammatory pathway and preserved RGCs.The uploaded files include:- Raw and normalized data from flat-mounted immunostaining (RGC and microglia counts), Western blot membranes (protein expression), TUNEL-stained cryosections (apoptosis), and Epon-embedded sections (NFL thickness and NDS evaluation).- Source data used to generate the figures.This dataset is made available to promote transparency and reproducibility in glaucoma research, particularly in studies involving retinal neuroinflammation and microglial modulation.
Authors
- Sato, Taimu ;
- Ishikawa, Makoto ;
- Izumi, Yukitoshi ;
- Shibata, Naoya ;
- Kota, Sato ;
- Ohno-Oishi, Michiko ;
- Tawarayama, Hiroshi ;
- Kunikata, Hiroshi ;
- Zorumski, Charles F. ;
- Nakawaza, Toru
This dataset supports the findings of the manuscript titled:"Involvement of microglia in retinal ganglion cell injury induced by IOP elevation in a rat ex vivo acute glaucoma model."In this study, we used a rat ex vivo model of acute intraocular pressure (IOP) elevation to investigate the role of microglia in retinal ganglion cell (RGC) injury. Our results demonstrate that pressure-induced activation of the TLR4-NLRP3 inflammasome cascade contributes to microglial proliferation and IL-1β production, leading to RGC apoptosis. Pharmacological depletion of microglia using the CSF-1R inhibitor PLX5622 suppressed this inflammatory pathway and preserved RGCs.The uploaded files include:- Raw and normalized data from flat-mounted immunostaining (RGC and microglia counts), Western blot membranes (protein expression), TUNEL-stained cryosections (apoptosis), and Epon-embedded sections (NFL thickness and NDS evaluation).- Source data used to generate the figures.This dataset is made available to promote transparency and reproducibility in glaucoma research, particularly in studies involving retinal neuroinflammation and microglial modulation.
Authors
- Sato, Taimu ;
- Ishikawa, Makoto ;
- Izumi, Yukitoshi ;
- Shibata, Naoya ;
- Kota, Sato ;
- Ohno-Oishi, Michiko ;
- Tawarayama, Hiroshi ;
- Kunikata, Hiroshi ;
- Zorumski, Charles F. ;
- Nakawaza, Toru
This dataset supports the findings of the manuscript titled:"Involvement of microglia in retinal ganglion cell injury induced by IOP elevation in a rat ex vivo acute glaucoma model."In this study, we used a rat ex vivo model of acute intraocular pressure (IOP) elevation to investigate the role of microglia in retinal ganglion cell (RGC) injury. Our results demonstrate that pressure-induced activation of the TLR4-NLRP3 inflammasome cascade contributes to microglial proliferation and IL-1β production, leading to RGC apoptosis. Pharmacological depletion of microglia using the CSF-1R inhibitor PLX5622 suppressed this inflammatory pathway and preserved RGCs.The uploaded files include:- Raw and normalized data from flat-mounted immunostaining (RGC and microglia counts), Western blot membranes (protein expression), TUNEL-stained cryosections (apoptosis), and Epon-embedded sections (NFL thickness and NDS evaluation).- Source data used to generate the figures.This dataset is made available to promote transparency and reproducibility in glaucoma research, particularly in studies involving retinal neuroinflammation and microglial modulation.
Authors
- Sato, Taimu ;
- Ishikawa, Makoto ;
- Izumi, Yukitoshi ;
- Shibata, Naoya ;
- Kota, Sato ;
- Ohno-Oishi, Michiko ;
- Tawarayama, Hiroshi ;
- Kunikata, Hiroshi ;
- Zorumski, Charles F. ;
- Nakawaza, Toru