Background and Purpose-A recent report has demonstrated that the contralesional primary motor cortex (M1) inhibited the ipsilesional M1 via an abnormal transcallosal inhibition (TCI) in stroke patients. We studied whether a decreased excitability of the contralesional M1 induced by 1 Hz repetitive transcranial magnetic stimulation (rTMS) caused an improved motor performance of the affected hand in stroke patients by releasing the TCI. Methods-We conducted a double-blind study of real versus sham rTMS in stroke patients. After patients had wellperformed motor training to minimize the possibility of motor training during the motor measurement, they were randomly assigned to receive a subthreshold rTMS at the contralesional M1 (1 Hz, 25 minutes) or sham stimulation. Results-When compared with sham stimulation, rTMS reduced the amplitude of motor-evoked potentials in contralesional M1 and the TCI duration, and rTMS immediately induced an improvement in pinch acceleration of the affected hand, although a plateau in motor performance had been reached by the previous motor training. This improvement in motor function after rTMS was significantly correlated with a reduced TCI duration. Conclusions-We have demonstrated that a disruption of the TCI by the contralesional M1 virtual lesion caused a paradoxical functional facilitation of the affected hand in stroke patients; this suggests a new neurorehabilitative strategy for stroke patients.

rTMS improved the motor learning of the affected hand in patients after stroke; thus, it can apply as anew rehabilitation strategy for patients after stroke.

Bilateral repetitive transcranial magnetic stimulation improved the motor training effect on the paretic hand of patients after stroke more than unilateral stimulation in pinch force; this might indicate a new neurorehabilitative strategy for stroke.

The ALL-1 gene is directly involved in 5-10% of acute lymphoblastic leukemias (ALLs) and acute myeloid leukemias (AMLs) by fusion to other genes or through internal rearrangements. DNA microarrays were used to determine expression profiles of ALLs and AMLs with ALL-1 rearrangements. These profiles distinguish those tumors from other ALLs and AMLs. The expression patterns of ALL-1-associated tumors, in particular ALLs, involve oncogenes, tumor suppressors, antiapoptotic genes, drug-resistance genes, etc., and correlate with the aggressive nature of the tumors. The genes whose expression differentiates between ALLs with and without ALL-1 rearrangement were further divided into several groups, enabling separation of ALL-1-associated ALLs into two subclasses. One of the groups included 43 genes that exhibited expression profiles closely linked to ALLs with ALL-1 rearrangements. Further, there were evident differences between the expression profiles of AMLs in which ALL-1 had undergone fusion to other genes and AMLs with partial duplication of ALL-1. The extensive analysis described here pinpointed genes that might have a direct role in pathogenesis.C hromosome band 11q23 is a region of recurrent rearrangements in human acute leukemias. These rearrangements, usually in the form of reciprocal chromosome translocations, affect 5-10% of children and adults with acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AML). The most common translocations are t(4;11) and t(9;11), accounting for 40% and 27%, respectively, of all 11q23 rearrangements. There is a strong association between leukemia phenotype and particular rearrangements. Thus, t(4;11) occurs nearly exclusively in ALL, and 85% of cases with t(9;11) are AMLs (1, 2). Essentially all 11q23 abnormalities involve the ALL-1 gene (also termed MLL, HRX, or HTRX), which rearranges with Ͼ30 partner genes to produce fusion proteins composed of ALL-1 N terminus and the C terminus of the partner protein (3, 4). A second and less frequent type of ALL-1 rearrangement does not involve partner genes but rather partial duplications of ALL-1 N-terminal segments (5). ALL-1-associated leukemias show some unusual and intriguing features (reviewed in refs. 6 and 7). First, they predominate infant acute leukemias, amounting to 80% of infants with ALL and 65% of those with AML. Second, they account for the majority of therapyrelated (secondary) leukemias, developing in 5-15% of primary cancer patients treated with drugs, such as etoposide (VP16), that inhibit DNA topoisomerase II. Third, in infant leukemia and in therapy-related leukemia the disease arises after a brief latency. In fact, studies of monozygotic twins and newborns with leukemia and analysis of neonatal blood spots from children who were diagnosed with leukemia indicate that in most or all infant leukemias ALL-1 rearrangements occur in utero. The short latency suggests that ALL-1 fusion proteins induce leukemia with few, if any, additional mutations. Fourth, prognosis of patients with 11q23 abnormalities is ...

Inhibitory rTMS over the unaffected hemisphere transiently caused deterioration of bimanual movements for the current task in stroke patients. This short-term decline was prevented by combined administration of low-frequency rTMS over the unaffected hemisphere and anodal tDCS over the affected hemisphere. These responses to bihemispheric stimulation suggest possible caution and opportunities for the rehabilitation of hand function after stroke.