Leukemia (2012) 26, 323-331; doi:10.1038/leu.2011.198; published online 5 August 2011″
“The role of the presence of others in a social context has been debated widely. Although the importance of mutual cognitive functions between performer and observer is generally accepted, little is known about the neural correlates of paired performers and observers themselves. In this near-infrared spectroscopy (NIRS) study we Selleckchem Sonidegib measured the activation in the bilateral inferior parietal lobule (IPL) when driver-observer pairs of participants

performed a driving video game task. The performer’s task was to drive from start to goal using a default route find more map, while their partner observed the performance. According to the performer’s subjective appraisal of the copresent observer obtained after the driving task, the pairs were divided into three groups: supportive, nonsupportive, and neutral. The driving time, error, and tension

score did not show significant differences between the three groups. However, NIRS data of performers in the supportive group showed significantly higher activation in the left IPL than those in the nonsupportive group, but not in the right IPL. NIRS data of observers in the concerned two groups did not show significant differences bilaterally in IPL. These results suggest that the left IPL distinctively responds according to a performer’s cognitive appraisal of a copresent observer. NeuroReport 23:835-839 (C) 2012 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.”
“Activation PDK3 of the fibrinolytic system during lymphoma progression is a well-documented clinical phenomenon. But the mechanism by which the fibrinolytic system can modulate lymphoma progression has been elusive.

The main fibrinolytic enzyme, plasminogen (Plg)/plasmin (Plm), can activate matrix metalloproteinases (MMPs), such as MMP-9, which has been linked to various malignancies. Here we provide the evidence that blockade of Plg reduces T-cell lymphoma growth by inhibiting MMP-9-dependent recruitment of CD11b(+)F4/80(+) myeloid cells locally within the lymphoma tissue. Genetic Plg deficiency and drug-mediated Plm blockade delayed T-cell lymphoma growth and diminished MMP-9-dependent CD11b(+)4/80(+) myeloid cell infiltration into lymphoma tissues. A neutralizing antibody against CD11b inhibited T-cell lymphoma growth in vivo, which indicates that CD11b(+) myeloid cells have a role in T-cell lymphoma growth. Plg deficiency in T-cell lymphoma-bearing mice resulted in reduced plasma levels of the growth factors vascular endothelial growth-A and Kit ligand, both of which are known to enhance myeloid cell proliferation.