[The clinical effect of combination therapy with edaravone and sodium ozagrel for acute cerebral infarction].

Sodium ozagrel (ozagrel), a selective thromboxane A2 synthetase inhibitor, has been used for the treatment of various types of acute ischemic stroke, except cardioembolic stroke. Recently, edaravone, a novel free radical scavenger, has been approved for the treatment of acute ischemic stroke within 24 hours after onset. Since these two drugs differ in mode of action, we hypothesized that combination of both drugs would yield further improvement of the outcome of patients with acute ischemic stroke. The clinical efficacy of combination therapy with edaravone and ozagrel for acute ischemic stroke was studied retrospectively, and compared with that of ozagrel alone. A total of 62 patients who suffered acute ischemic stroke within 24 hours after onset during the 10-month period from June 2001 to March 2002, were treated with both edaravone and ozagrel (E-O group), while 76 patients during August 2000 to May 2001, were treated with ozagrel alone (O group). The rate of modified Rankin Scale (MRS) 0 and 1 at discharge in the total ischemic stroke and atherothrombotic stroke, was significantly higher in the E-O group than in the O group. The improvement in MRS also differed between E-O group and O group in total. The difference was significant in patients with atherothrombotic stroke but not in those with lacunar stroke. These results indicate that combination therapy with edaravone and ozagrel is more effective than mono-therapy with ozagrel for the treatment of acute ischemic, especially of atherothrombotic stroke.

Molecular analysis of the rhabdoid predisposition syndrome in a child: a novel germline hSNF5/INI1 mutation and absence of c-myc amplification.

The authors report a case of the rhabdoid predisposition syndrome (RPS) secondary to a germline hSNF5/INI1 mutation, whose brain tumor was originally unclassified but finally diagnosed as an atypical teratoid/rhabdoid tumor (AT/RT) by molecular analysis. A 7-month-old infant presented with hydrocephalus secondary to a huge pineal tumor and subsequently developed a renal rhabdoid tumor. The histology of the brain tumor was initially undetermined; however, an AT/RT was strongly suspected because of her clinical course. Mutational screening of the hSNF5/INI1 gene by heteroduplex and direct sequence analysis detected a missense mutation at codon 53 (CGA --> TGA, arginine --> stop) in both tumors, as well as in normal tissue of the kidney. Polymerase chain reaction (PCR)-based microsatellite analysis showed in both tumors allelic loss on chromosome arm 22q to which the hSNF5/INI1 gene maps. c-myc amplification was examined by differential PCR but not detected. Histologic review of the brain tumor by immunohistochemistry confirmed focal expression of epithelial membrane antigen and smooth muscle actin. These findings suggest that the brain tumor was really an AT/RT as a component of RPS secondary to a germline hSNF5/INI1 mutation. The present mutation has never been reported in the literature.