thalidomide has been researched along with Infarction, Middle Cerebral Artery in 3 studies
Thalidomide: A piperidinyl isoindole originally introduced as a non-barbiturate hypnotic, but withdrawn from the market due to teratogenic effects. It has been reintroduced and used for a number of immunological and inflammatory disorders. Thalidomide displays immunosuppressive and anti-angiogenic activity. It inhibits release of TUMOR NECROSIS FACTOR-ALPHA from monocytes, and modulates other cytokine action.
thalidomide : A racemate comprising equimolar amounts of R- and S-thalidomide.
2-(2,6-dioxopiperidin-3-yl)-1H-isoindole-1,3(2H)-dione : A dicarboximide that is isoindole-1,3(2H)-dione in which the hydrogen attached to the nitrogen is substituted by a 2,6-dioxopiperidin-3-yl group.
Infarction, Middle Cerebral Artery: NECROSIS occurring in the MIDDLE CEREBRAL ARTERY distribution system which brings blood to the entire lateral aspects of each CEREBRAL HEMISPHERE. Clinical signs include impaired cognition; APHASIA; AGRAPHIA; weak and numbness in the face and arms, contralaterally or bilaterally depending on the infarction.
| Excerpt | Relevance | Reference |
|---|---|---|
| "Apremilast (APR) is a selective inhibitor of phosphodiesterase-4 involved in various neurological diseases, including stroke." | 5.72 | Apremilast exerts protective effects on stroke outcomes and blood-brain barrier (BBB) dysfunction through regulating Rho-associated protein kinase 2 expression. ( Cheng, Z; Meng, X; Wang, M, 2022) |
| "Apremilast (APR) is a selective inhibitor of phosphodiesterase-4 involved in various neurological diseases, including stroke." | 1.72 | Apremilast exerts protective effects on stroke outcomes and blood-brain barrier (BBB) dysfunction through regulating Rho-associated protein kinase 2 expression. ( Cheng, Z; Meng, X; Wang, M, 2022) |
| "Thalidomide treatment significantly decreased the infarct volume and neurological deficits of MCAO/R rats." | 1.48 | The Neuroprotective Effect of Thalidomide against Ischemia through the Cereblon-mediated Repression of AMPK Activity. ( Asahi, T; Fujiwara, M; Hayashi, H; Sawamura, N; Takagi, N; Yamada, H; Yamada, M, 2018) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 1 (33.33) | 29.6817 |
| 2010's | 1 (33.33) | 24.3611 |
| 2020's | 1 (33.33) | 2.80 |
| Authors | Studies |
|---|---|
| Wang, M | 1 |
| Meng, X | 1 |
| Cheng, Z | 1 |
| Sawamura, N | 1 |
| Yamada, M | 1 |
| Fujiwara, M | 1 |
| Yamada, H | 1 |
| Hayashi, H | 1 |
| Takagi, N | 1 |
| Asahi, T | 1 |
| Hyakkoku, K | 1 |
| Nakajima, Y | 1 |
| Izuta, H | 1 |
| Shimazawa, M | 1 |
| Yamamoto, T | 1 |
| Shibata, N | 1 |
| Hara, H | 1 |
3 other studies available for thalidomide and Infarction, Middle Cerebral Artery
| Article | Year |
|---|---|
Apremilast exerts protective effects on stroke outcomes and blood-brain barrier (BBB) dysfunction through regulating Rho-associated protein kinase 2 expression.
Topics: Animals; Blood-Brain Barrier; Brain Ischemia; Claudin-5; Cyclic Nucleotide Phosphodiesterases, Type | 2022 |
The Neuroprotective Effect of Thalidomide against Ischemia through the Cereblon-mediated Repression of AMPK Activity.
Topics: AMP-Activated Protein Kinases; Animals; ATP-Dependent Proteases; Brain Ischemia; Cell Death; Cell Li | 2018 |
Thalidomide protects against ischemic neuronal damage induced by focal cerebral ischemia in mice.
Topics: 8-Hydroxy-2'-Deoxyguanosine; Analysis of Variance; Animals; Blood Pressure; Cell Death; Cells, Cultu | 2009 |