Compared with FDG PET in glioma, MET PET was an independent significant prognostic factor and MET uptake was correlated with cellular proliferation. MET PET may be a useful biological prognostic marker in glioma patients.

Objective-There is hope that molecular imaging can identify vulnerable atherosclerotic plaques. However, there is a paucity of clinical translational data to guide the future development of this field. Here, we cross-correlate cathepsin-B or matrix metalloproteinase-2/-9 molecular optical imaging data of human atheromata or emboli with conventional imaging data, clinical data, and histopathologic data. Methods and Results-Fifty-two patients undergoing carotid endarterectomy (41 atheromata) or carotid stenting (15 captured emboli) were studied with protease-activatable imaging probes. We show that protease-related fluorescent signal in carotid atheromata or in emboli closely reflects the pathophysiologic alterations of plaque inflammation and statin-mediated therapeutic effects on plaque inflammation. Inflammation-related fluorescent signal was observed in the carotid bifurcation area and around ulcero-hemorrhagic lesions. Pathologically proven unstable plaques had high cathepsin-B-related fluorescent signal. The distribution patterns of the mean cathepsin-B imaging signals showed a difference between the symptomatic vs asymptomatic plaque groups. However, the degree of carotid stenosis or ultrasonographic echodensity was weakly correlated with the inflammatory proteolytic enzyme-related signal, suggesting that molecular imaging yields complimentary new information not available to conventional imaging. Key Words: atherosclerosis Ⅲ cathepsin-B Ⅲ molecular imaging Ⅲ protease Ⅲ structural imaging C onventional imaging approaches such as angiography and ultrasound offer primarily structural information and yields limited data on plaque stability. The degree of carotid stenosis, as determined by structural imaging, is currently the most important therapeutic parameter in deciding on vascular intervention in addition to medical treatment. 1 There is hope that the emerging technologies of molecular imaging could provide a window of insight into the underlying molecular processes that give rise to plaque rupture. [2][3][4] Vulnerable plaques are characterized by the presence of inflammatory mediators and proteolytic enzymes, such as cathepsins and matrix metalloproteinases, which disturb the structural integrity of atheromatous plaques and consequently provoke plaque rupture to expose the lipid-rich plaque interior to thrombin-activating blood cascades. [5][6][7] It is the presence of these molecular species that distinguishes stable atheromatous lesions from unstable ones. We chose to leverage these molecular differences by devising imaging agents to probe for these enzymes. Conclusion-TheseWe and others 2,3,8,9 have developed protease-sensing nearinfrared fluorescent (NIRF) molecular imaging agents that are optically silent at injection because of auto-quenching between closely spaced fluorochromes. After enzyme-specific proteasemediated cleavage, fluorochromes are dequenced and become brightly fluorescent. 2,3,8,9 This technology has potential clinical applicability when combined with an intraoperative NIRF imaging...

Ischemic dysfunction of the frontal cortical and subcortical motor pathways rather than that of the basal ganglia was suspected to be the cause of the observed contralateral involuntary movements. Direct and indirect bypass surgery can be used effectively to treat involuntary movements in patients with cerebral ischemic diseases such as MMD and in those with stenosis of an intracranial major artery.

When hematoma size was similar, iNOS knockout mice had significantly less brain edema than their littermates. These results suggest that iNOS modulation might become an antiedematous therapy for ICH.