Browsing by Subject "Cerebral infarction"

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    Lectin , UEA- 1, reaction of capillary endothelium with reference to permeability in autopsied cases of cerebral infarction
    (Murcia : F. Hernández, 1986) Eizi Kadota; Kurenai Tanji; Shozo Nishida; Manabu Takahashi; Mitsuyo Maeda; Shingo Hiruma; Yoshiki Enomoto; Shigeo Hashimoto; Fumiharu Akai
    The relationship between endothelial reactivity to Ulex europaeus agglutinin-1 (UEA-I) and the permeability of the vascular wall in human autopsied cases ol' cerebral infarction was studied. Sections from the cerebral cortex were reacted with horseradish peroxidase UEA-1 to demonstrate the surface membrane of endothelial cells. Albumin in the neuropil of sections was de~nonstrated for the estimation of increased vascular permeability. The results showed that endothelial reactivity to UEA-I was reduced in cases where death had occurred 3 to 5 days after onset of cerebral infarction. Reactivity was also diminished in cases where death had occurred after 13 and 25 days; these cases showed fresh ischemic lesions caused by reattacks of infarction. Albumin extravasation into the neuropil was demonstrated in these intermediate cases. Chronic cases, dying after more than 52 days, showed no reduction of endothelial reactivity to UEA-I and no albumin extravasation was proved. It was concluded that UEA-1 can be employed as a useful n~orphological marker for evaluation of endothelial function and vascular permeability.
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    Time-dependent and lesion-dependent HMGB1-selective localization in brains of patients with cerebrovascular diseases
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Umahara, Takahiko; Uchihara, Toshiki; Hirokawa, Katsuiku; Hirao, Kentaro; Shimizu, Soichiro; Hashimoto, Takao; Terasi, Hiroo; Hanyu, Haruo
    High mobility group box 1 protein (HMGB1) has multiple functions, including the maintenance of nucleosomes and the regulation of gene transcription. HMGB1 is released from activated macrophages, resulting in the induction of inflammatory cytokines. Recently, much research about the role of HMGB1 in cerebrovascular disease (CVD) has been reported. In an animal model, HMGB1 neutralization ameliorates brain infarction, there is an early release of HMGB1 from neurons, and HMGB1 antibody attenuates delayed cerebral vasospasm in experimental subarachnoid hemorrhage. It was also reported that elevation of HMGB1 in serum correlates with severity of acute intracerebral hemorrhage. However, the evidence of HMGB1 localization in brains of patients with CVD is very limited. Therefore, we investigated at autopsy the immunolocalization of HMGB1 in brains of patients with CVD (acute and chronic cerebral infarction, acute cerebral hemorrhage, subarachnoid hemorrhage). In 3 out of 10 acute cerebral infarction cases, the cytoplasm of neurons located around the ischemic core (i.e., penumbra) was positive for HMGB1. In the chronic stage of cerebral infarction, macrophages located in some ischemic regions were positive for HMGB1. Around the hematoma in the basal ganglia, HMGB1-like immunoreactivity (IR) was intense in macrophages. However, around the subarachnoid hematoma, HMGB1- like IR was not seen in the cortex. In arteries surrounded by subarachnoid hematoma, HMGB1-like IR was located in the cytoplasm of vascular smooth muscle cells. These findings, which partially differ from animal model results, may provide translational research and a basis for understanding the role of HMGB1 in brains of patients with CVD.