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Thrombin-induced kynurenine 3-monooxygenase causes variations in the kynurenine pathway, leading to neurological deficits in a murine intracerebral hemorrhage model.

J Pharmacol Sci

February 2025

Department of Physical Chemistry for Bioactive Molecules, Faculty of Pharmacy and Pharmaceutical Sciences, Fukuyama University, 985-1 Sanzo, Higashimura-cho, Fukuyama, Hiroshima, 729-0292, Japan.

The purpose of the present study is to investigate changes in the kynurenine pathway after intracerebral hemorrhage (ICH) and its effects on ICH-induced injury. The exposure of a primary rat microglial culture to thrombin increased the mRNA level of kynurenine 3-monooxygenase (KMO), and this increase was attenuated by a p38 MAPK inhibitor. Thrombin also increased the protein level of KMO.

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Background: Intracranial hemorrhage (ICH) is a devastating stroke subtype with a high rate of mortality and disability. Therapeutic options available are primarily limited to supportive care and blood pressure control, whereas the surgical approach remains controversial. In this study, we explored the effects of noninvasive vagus nerve stimulation (nVNS) on hematoma volume and outcome in a rat model of collagenase-induced ICH.

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Intracerebral hemorrhage (ICH) and perihematomal edema (PHE) are key imaging markers of primary and secondary brain injury in hemorrhagic stroke. Accurate segmentation and quantification of ICH and PHE can help with prognostication and guide treatment planning. In this study, we combined Swin-Unet Transformers with nnU-NETv2 convolutional network for segmentation of ICH and PHE on non-contrast head CTs.

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: Intracerebral hemorrhages (ICH) and perihematomal edema (PHE) are respective imaging markers of primary and secondary brain injury in hemorrhagic stroke. In this study, we explored the potential added value of PHE radiomic features for prognostication in ICH patients. : Using a multicentric trial cohort of acute supratentorial ICH ( = 852) patients, we extracted radiomic features from ICH and PHE lesions on admission non-contrast head CTs.

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Inhibition of Bruton's tyrosine kinase restricts neuroinflammation following intracerebral hemorrhage.

Theranostics

January 2025

Department of Neurology, Tianjin Neurological Institute, Tianjin Institute of Immunology, State Key Laboratory of Experimental Hematology, International Joint Laboratory of Ocular Diseases, Ministry of Education, Haihe Laboratory of Cell Ecosystem, Laboratory of Post-Neuroinjury Neurorepair and Regeneration in Central Nervous System Tianjin & Ministry of Education, Tianjin Medical University General Hospital, Tianjin 300052, China.

Intracerebral hemorrhage (ICH) is a devastating form of stroke with a lack of effective treatments. Following disease onset, ICH activates microglia and recruits peripheral leukocytes into the perihematomal region to amplify neural injury. Bruton's tyrosine kinase (BTK) controls the proliferation and survival of various myeloid cells and lymphocytes.

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