Hepatocyte transplantation is restricted by the impaired ability of hepatocytes to engraft and survive in the damaged liver. Understanding the mechanisms that control this process will permit the development of strategies to improve engraftment. We studied changes in liver matrix during acute injury and delineated the mechanisms that perturb the successful adhesion and engraftment of hepatocytes. Collagen IV expression was increased in sinusoidal endothelium and portal tracts of fulminant hepatic failure explants, whereas there were minimal changes in the expression of fibronectin, tenascin, and laminin. Using an in vitro model of cellular adhesion, hepatocytes were cultured on collagen-coated plates and exposed to serum from patients with liver injury to ascertain their subsequent adhesion and survival. There was a rapid, temporally progressive decrease in the adhesive properties of hepatocytes exposed to such serum that occurred within 4 hours of exposure. Loss of activity of the 1-integrin receptor, which controls adhesion to collagen, was seen to precede this loss of adhesive ability. Addition of the 1-integrin activating antibody (TS2/16) to cells cultured with liver injury serum significantly increased their adhesion to collagen, and prevented significant apoptosis. In conclusion, we have identified an important mechanism that underpins the failure of infused hepatocytes to engraft and survive in liver injury. Pretreating cells with an activating antibody can improve their engraftment and survival, indicating that serum from patients with liver injury exerts a defined nontoxic biological effect. This finding has important implications in the future of cellular transplantation for liver and other organ diseases. (HEPATOLOGY 2004;40:636 -645.)
Atypical teratoid/rhabdoid (AT/RT) tumor is a rare, highly malignant tumor of the central nervous system (CNS), most commonly found in children less than 5 years of age. Although the vast majority of cases are diagnosed in young children, there have been isolated case reports in adults. Since its histological appearance can be confused with other tumors, especially in adults, separating AT/RT from other neoplasms may be difficult. In many instances, a reliable diagnosis is not possible without demonstrating the lack of nuclear INI1 (SMARCB1) or BRG1 (SMARCA4) protein expression by immunohistochemical methods or by detection of somatic / germline mutation of the INI1 (SMARCB1) or BRG1 (SMARCA4) gene. Final diagnosis is confirmed after immunohistochemical analysis and/or molecular analysis. Immunohistochemical staining show that the tumor cells are positive for vimentin and reacted variably for keratin, epithelial membrane antigen (EMA), synaptophysin, neurofilament protein, CD34, and smooth muscle actin (SMA) and negative for GFAP, S-100, desmin and CD99. In adult examples of AT/RT, the diagnosis requires a high index of suspicion, with early tissue diagnosis and a low threshold for investigation with INI1 immunohistochemistry to differentiate this entity from other morphologically similar tumors. Although
Cystic meningioma refers to meningothelial neoplasms or meningiomas associated with cyst formation. Clinical features depend on the tumors' size and location, and include symptoms of increased intracranial pressure, seizures, and focal neurological deficit. Four types of cystic meningiomas are described in the literature, suggested by Nauta et al., based on radiologic findings: Type I: Intratumoral cysts in which the tumor, macroscopically visible on all sides of the cyst, surrounds the cavity; Type II: Intratumoral cysts, lying at the periphery of the tumor and surrounded by a row of neoplastic cells, detectable microscopically; Type III: Peritumoral cysts, whose walls consisted partly of adjacent parenchyma and partly of the tumor; and Type IV: Peritumoral cysts, whose walls are formed by the arachnoid (arachnoid cyst), separated from the tumor by a distinct capsule. Theories proposed to explain cyst formation include degeneration or necrosis, direct secretion by meningioma, and reactive changes (peripheral arachnoid cysts). The tumor itself has features similar to non-cystic meningiomas. The cysts are usually of variable size and can be entirely surrounded by tumor (types I or II), clearly between the tumor and the brain (type IV), or within the adjacent brain (type III). On imaging, it is sometimes difficult to distinguish between these types. We herewith present two cases of cystic meningiomas.
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