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Role of Hyperintense Acute Reperfusion Marker for Classifying the Stroke Etiology.

ABSTRACT: The hyperintense acute reperfusion marker (HARM) is a delayed enhancement of the subarachnoid or subpial space observed on post-contrast fluid-attenuated inversion recovery (FLAIR) images and is associated with permeability changes to the blood-brain barrier in acute stroke. We investigated the relationship between HARM and stroke etiology based on the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) classification. In addition, we evaluated the relationship between HARM and stroke locations with respect to vascular territories and anatomic compartments.We recruited 264 consecutive patients (109 women; mean age 68.63?years) who were diagnosed with acute ischemic stroke and underwent brain magnetic resonance imaging (MRI) including post-contrast FLAIR and DWI within 7?days of symptom onset from May 2015 to March 2016 for this retrospective study. Post-contrast FLAIR images were obtained 5?min after gadolinium administration. The mean time interval between the onset of stroke symptoms and MRI acquisition in total included patients was 18?h and 7?min (median 12?h and 57?min, range 2-127?h). We analyzed the overall incidence and distribution patterns of HARM in acute ischemic stroke cases and compared the relative incidence and distribution patterns of HARM between the subgroups of stroke etiology based on conventional TOAST classification. We obtained odds ratio (OR) of HARM in different stroke locations based on vascular territories and anatomical compartments. This study was approved by our institutional review board.Among the 264 patients, 67 (25.38%) patients were HARM positive and 197 (74.62%) patients were HARM negative. There was significant difference in HARM incidence among the stroke subgroups (p?

SUBMITTER: Choi HY

PROVIDER: S-EPMC5727375 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

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Role of Hyperintense Acute Reperfusion Marker for Classifying the Stroke Etiology.

Choi Hee Young HY Lee Kyung Mi KM Kim Hyug-Gi HG Kim Eui Jong EJ Choi Woo Suk WS Kim Bum Joon BJ Heo Sung Hyuk SH Chang Dae-Il DI

Frontiers in neurology 20171129

<h4>Purpose</h4>The hyperintense acute reperfusion marker (HARM) is a delayed enhancement of the subarachnoid or subpial space observed on post-contrast fluid-attenuated inversion recovery (FLAIR) images and is associated with permeability changes to the blood-brain barrier in acute stroke. We investigated the relationship between HARM and stroke etiology based on the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) classification. In addition, we evaluated the relationship between HARM and ...[more]

PMID: 29276498

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Project description:BACKGROUND:To establish a model of chronic renal fibrosis following acute kidney injury (AKI) in BALB/c mice and to observe the effect of AKI on podocyte injury and chronic fibrosis of the kidney. Additional aims included using the model to explore the role of podocyte injury in AKI and post-injury fibrosis. METHODS:Fifty BALB/C mice were randomly divided into control group (Ctr), sham group (sham), AKI 20 group (renal ischemia, 20 min reperfusion), AKI 30 group (renal ischemia, 30 min reperfusion) and AKI 40 group (renal ischemia, 40 min reperfusion). Mice serum and 24-h urine were collected on the 8th, 9th, 10th, 14th, and 28th days for urinary protein, serum creatinine (Scr) and blood urea nitrogen (BUN) analysis. HE staining, transmission electron microscopy (TEM), Masson staining, Q-PCR, Western Blot and immunohistochemistry were applied. RESULTS:Serum Scr and BUN levels across all AKI groups at the 9th day were significantly higher (P < 0.05) than controls, with higher reperfusion groups maintaining that increase up to 28 days (P < 0.05). Compared with Ctr group, the urinary protein of the AKI 40 group significantly rose on the 9th day (P < 0.05), normalizing immediately on the 10th day (P < 0.05). In contrast, the AKI 30 group rose significantly on the 14th day (P < 0.05) maintaining elevated levels for two weeks (P < 0.05). HE staining demonstrated ischemia-dependent renal tissue damage was aggravated in the mild to aggravated AKI groups. Mesangial proliferation, glomerulosclerosis, and tubulointerstitial pathology were also significantly increased in these groups (P < 0.05). Masson staining further showed that glomerular, renal tubular, and interstitial collagen were increased by ischemia in a time-dependent manner. Transmission EM additionally that podocytes of the mild to severe AKI groups displayed extensive fusion, exfoliation and GBM exposure. Synaptopodin, Nephrin, and CD2AP mRNA and protein expression demonstrated ischemic time-dependent decreases, while the TRPC6 was increased. There was a significant difference in the levels of Synaptopodin, Nephrin, CD2AP, and TRPC6 between the mild and severe AKI groups (P < 0.05). CONCLUSIONS:1) During the AKI process mice podocyte injury, proteinuria and the subsequent progression into chronic renal fibrosis is observed.2) Podocyte injury may be one of the causes of ischemia-reperfusion acute kidney injury and post-injury fibrosis.

Dataset Information

Role of Hyperintense Acute Reperfusion Marker for Classifying the Stroke Etiology.

Publications

Role of Hyperintense Acute Reperfusion Marker for Classifying the Stroke Etiology.

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