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Katsumi Hoya

Publications and source records attributed to Katsumi Hoya.

4 recordsLinked to original sources
PubMed2006

Nestin expression in vascular malformations: a novel marker for proliferative endothelium.

Cavernous angiomas (CAs) and arteriovenous malformations (AVMs) sometimes show growth or de novo appearance. Proliferative capacity of the endothelium is evident in such malformations. Intermediate filament nestin is a newly identified marker for proliferative endothelium, which was originally detected in the neuroepithelial stem cells of the embryonal central nervous system. Immunohistochemical analysis of nestin was evaluated as a marker for proliferative capacity of endothelial cells by comparison with proliferating cell nuclear antigen (PCNA). Sixteen of 27 CAs and 13 of 20 AVMs were positive for nestin. Likewise, 12 of 27 CAs and 10 of 20 AVMs were positive for PCNA. Nestin staining was stronger in the typical malformative vessels of CAs than in AVMs, in both the endothelial cells and the interstitial cells. Newly formed endothelial cells expressed nestin strongly in the reactive tissues including organizing or encapsulated hematomas. These results suggest that neovascularization occurs in the process of repeated bleeding and remodeling of hematomas.

Adolescent↗
PubMed2005

Basilar artery dissection.

OBJECT: Little is understood about the clinical manifestations of basilar artery (BA) dissections, which can present with subarachnoid hemorrhage (SAH), brainstem compression, or ischemia. In any instance, the prognosis seems poorer than that for vertebral artery (VA) dissection. The authors analyzed clinical presentations and radiological features of BA dissection with and without rupture. METHODS: Between 1998 and 2003, the authors treated 10 patients (eight men and two women, ranging in age from 32-78 years; mean age 54 years) with BA dissection. Diagnosis was based on clinical and radiological findings, including those from magnetic resonance imaging and cerebral angiography studies. Of the 10 patients, five had impaired consciousness at disease onset. Among four patients presenting with SAH, two were treated conservatively and had fair outcomes without recurrent hemorrhage. The other two patients with SAH were treated using unilateral endovascular VA occlusion, but one of them subsequently suffered fatal rebleeding. A fifth patient presented with progressive signs of a mass involving the brainstem, whereas the remaining five patients showed brainstem ischemia; all were treated conservatively. Four patients could not return to their previous daily activities. CONCLUSIONS: Basilar artery dissections are rare lesions associated with significant morbidity and death. The natural course of and the treatment options for BA dissection differ considerably from those for VA dissections. Management of these lesions is controversial and difficult, and requires particular care.

Adult↗
PubMed2003

Expression of myosin heavy chain isoforms by smooth muscle cells in cerebral arteriovenous malformations.

We have characterised the blood vessels found in normal cerebral vasculature and in arteriovenous malformations (AVMs), based on the expression of smooth muscle cell (SMC)-specific proteins. The marker proteins used were smooth muscle alpha-actin and four myosin heavy chain isoforms (SM1, SM2, SMemb and NMHC-A). Specimens of AVM obtained during surgery, and normal cerebral vessels from autopsy cases were studied immunohistochemically and compared. The arterial components of AVM contained an abundance of SMCs of the contractile phenotype, which were positive for alpha-actin, SM1 and SM2, but not for SMemb and NMHC-A. These components showed the same staining pattern as mature normal arteries. Two different types of abnormal veins were found in the AVM specimens: large veins with a thick and fibrous wall (so-called 'arterialised' veins) and intraparenchymal thin-walled sinusoidal veins. The former expressed alpha-actin, SM1, SM2, and SMemb, the latter expressed alpha-actin, SM1, and SM2. These marker expression patterns resembled those of normal cerebral arteries, and the results were compatible with arterialisation of the cerebral veins caused by arteriovenous shunting. However, the expression of SMemb was found only in the arterialised type of veins, not in the sinusoidal type or the arteries that had sustained abnormal blood flow in the AVMs. The thick-walled veins in the AVMs showed the same staining pattern as normal veins of dural plexus origin (large subarachnoid veins and dural sinuses). It is therefore possible to assume that they originated from the dural plexus, and extended into the brain during the formation of AVMs.

Actins↗