ABSTRACT
BACKGROUND: Compared to those found in the vertebrobasilar system, intracranial dissection in the anterior circulation is relatively rare, especially in the anterior cerebral artery (ACA). Moreover, only several cases of ACA dissection that underwent endovascular treatment have been reported. Here we present a rare case of gradually developing ACA dissecting aneurysm causing cerebral infarction, successfully treated by stent-assisted coil embolization. CASE DESCRIPTION: A 36-year-old man was admitted with sudden right hemiparesis. Diffusion-weighted magnetic resonance (MR) imaging showed cerebral infarction in the left ACA territory, and MR angiography showed segmental stenosis at the A2 portion of the left ACA. Three-dimensional digital subtraction angiogram showed segmental dilatation and stenosis at the left A2 portion. We diagnosed ACA dissection causing acute cerebral infarction and treated the patient conservatively. Five months after the onset, the dissecting artery at the left A2 portion formed a gradually dilating aneurysm, suggesting increased risk for aneurysmal rupture. We attempted endovascular treatment entailing coil embolization of an aneurysm while preserving the left A2 with stent assistance. The patient remained neurologically stable 6 months after the procedure. CONCLUSIONS: Although there are few reported cases of ACA dissection where endovascular treatment was attempted, we consider stent-assisted embolization for gradually developing ACA dissecting aneurysm as an alternative method to prevent bleeding and recurrent infarction.
ABSTRACT
We investigated c-Met expression in cultured astrocytes and their regulation by cytokines. Immunocytochemistry revealed that c-Met was expressed in cultured astrocytes. Western blotting revealed that acidic and basic fibroblast growth factor (FGF) enhanced and hepatocyte growth factor (HGF) reduced c-Met expression. Reverse transcription-polymerase chain reaction revealed that FGFs and HGF enhanced c-met expression. These findings suggest that c-Met expressed in astrocytes may have important roles during the nervous system regeneration.
Subject(s)
Astrocytes/physiology , Cytokines/pharmacology , Proto-Oncogene Proteins c-met/genetics , Animals , Animals, Newborn , Cells, Cultured , Epidermal Growth Factor/pharmacology , Fibroblast Growth Factor 1/pharmacology , Fibroblast Growth Factor 2/pharmacology , Hepatocyte Growth Factor/pharmacology , Interleukin-1/pharmacology , Nerve Regeneration , Rats , Rats, Wistar , Reverse Transcriptase Polymerase Chain Reaction , Tumor Necrosis Factor-alpha/pharmacologyABSTRACT
Patched (Ptc) is a transmembrane receptor for sonic hedgehog (Shh) and functionally associated with another transmembrane protein, smoothened (Smo). Ptc is a tumor suppressor gene whereas Smo serves as a proto-oncogene of neuroectodermal tumors. Their downstream molecules, Gli1, Gli2, and Gli3, are oncogenes of glioblastomas. We have analyzed mRNA expression of Ptc, Smo, and Gli family members in human astrocytic tumors. The mRNA expression was quantified by real-time polymerase chain reactions in 40 tumors (diffuse astrocytomas; 6 cases: anaplastic astrocytomas; 12 cases: glioblastomas; 22 cases) and four cell lines derived from astrocytic tumors. The MIB-1 proliferating cell indices (PCIs) of these tumors were analyzed by immunohistochemistry. In comparison with the World Health Organization (WHO) classification, the amount of Ptc and Smo mRNAs decreased in proportion to the progression of histological maliganancy, and similar results were obtained with astrocytic tumor-derived cell lines. However, there was no remarkable correlation between the mRNA expression level of each gene and the MIB-1 PCIs. The mRNA expression level of Gli1 was variable and highly elevated in two cases. No remarkable features were found clinically or histologically in these two cases. In summary, our results indicate that Ptc and Smo mRNA levels have an inverse correlation with histological malignancy and suggest that these gene products are implicated in the suppression of astrocytic tumors. In contrast, there was no significant correlation between the mRNA levels of the Gli family members and histological malignancy, suggesting that Gli proteins are not associated with the progression of astrocytic tumors.
Subject(s)
Astrocytoma/genetics , Astrocytoma/pathology , Brain Neoplasms/genetics , Brain Neoplasms/pathology , Membrane Proteins/biosynthesis , Oncogene Proteins/biosynthesis , Receptors, Cell Surface/biosynthesis , Receptors, G-Protein-Coupled , Transcription Factors/biosynthesis , Adult , Astrocytoma/metabolism , Biomarkers, Tumor , Brain Neoplasms/metabolism , Child , Female , Hedgehog Proteins , Humans , Immunohistochemistry , Infant , Ki-67 Antigen/metabolism , Male , Neoplasm Invasiveness , Patched Receptors , Polymerase Chain Reaction , Proto-Oncogene Mas , RNA, Messenger/analysis , Signal Transduction , Smoothened Receptor , Trans-Activators/metabolism , Zinc Finger Protein GLI1ABSTRACT
An extra-axial nodule in the cerebello-medullary fissure is described, occurring in a 27-year-old-woman. MRI and CT scans revealed the lesion was a non-enhanced round mass, which was associated with mild atrophy of the surrounding cerebellum, but with no perifocal edema. In the surgical observation, the mass was white, elastic and hard, well demarcated and localized in the cerebello-medullary fissure. Histologically, the lesion was composed of astrocytes and collagen-producing fibroblasts with no anaplasia. These findings suggested that the lesion was hamartomatous, but not neoplastic. This type of gliofibrous nodule has not been previously reported.
