RESUMO
Encapsulated acute subdural hematoma (ASDH) has been uncommonly reported. To our knowledge, a few cases of lentiform ASDH have been reported. The mechanism of encapsulated ASDH has been studied but not completely clarified. Encapsulated lentiform ASDH on a computed tomography (CT) scan mimics acute epidural hematoma (AEDH). Misinterpretation of biconvex-shaped ASDH on CT scan as AEDH often occurs and is usually identified by neurosurgical intervention. We report a case of an 85-year-old man presenting with a 2-day history of mental deterioration and right-sided weakness. CT scan revealed a biconvex-shaped hyperdense mass mixed with various densities of blood along the left temporoparietal cerebral convexity, which was misinterpreted as AEDH preoperatively. Emergency craniectomy was performed, but no AEDH was found beneath the skull. In the subdural space, encapsulated ASDH was located. En block resection of encapsulated ASDH was done. Emergency craniectomy confirmed that the preoperatively diagnosed AEDH was an encapsulated ASDH postoperatively. Radiologic studies of AEDH-like SDH allow us to establish an easy differential diagnosis between AEDH and ASDH by distinct features. More histological studies will provide us information on the mechanism underlying encapsulated ASDH.
RESUMO
Serum response factor (SRF) regulates transcription of the immediate early genes and triggers proliferation, migration and differentiation in several types of cells. We examined the role of SRF in HCC by transfecting the SRF cDNA in HLE cells and the SRF anti-sense cDNA in sarcomatoid HCC cells. The overexpression of SRF in the HLE cells significantly increased the cell growth and proliferation. Overexpression of SRF increased actin polymerization of the HCC cells and induced morphologic changes. The mesenchymal markers vimentin, N-cadherin and RhoA were highly expressed in the SRF-transfected HLE cells. Furthermore, the overexpression of SRF in the HLE cells increased the expression levels of the active form of the beta-catenin and Wnt/beta-catenin target genes, such as c-myc and cyclin D1. The overexpression of SRF significantly enhanced the cell migration and invasiveness of HCC cells. Conversely, inhibition of the SRF expression in the sarcomatoid SH-J1 cells by the SRF anti-sense cDNA significantly decreased migration and invasion through the attenuated expression of mesenchymal markers and the proteins involved in the Wnt/beta-catenin pathway. These results indicate that the overexpression of SRF in HCC cells modulates the Wnt/beta-catenin pathway, and this plays an important role in HCC progression.
