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Wang Y.,Oilfield General Hospital of Daqing | Liu B.,Oilfield General Hospital of Daqing | Fu L.,Oilfield General Hospital of Daqing | Cui Z.,Chinese PLA General Hospital
Journal of the Neurological Sciences | Year: 2015

We assessed the efficacy of interictal 18F-fluorodeoxyglucose (FDG)-positron emission tomography (PET) and magnetoencephalography (MEG) for localizing the epileptogenic foci in a small cohort of patients with non-lesional epilepsy. Sixteen patients, aged 8-32 years, with non-lesional epilepsy underwent MRI, continuous scalp video-electroencephalography (EEG) monitoring, interictal (FDG)-PET and MEG at our institution. Each patient subsequently underwent intracranial grid placement. The data from the intracranial grids was correlated with the previous studies to determine the efficacy of FDG-PET and MEG in localizing the epileptogenic zone. Of the 16 patients, the epileptogenic zone was accurately localized in 8 (50%) using FDG-PET and in 12 patients (75%) using MEG. Of the 11 patients with a temporal hypometabolism, only 4 were ultimately confirmed as temporal lobe epilepsy via intracranial grids and 2 additional patients were found to have extra-temporal lobe epilepsy. Compared to interictal FDG-PET, MEG appears to be more sensitive to detection of the epileptogenic zone in this small cohort of non-lesional epilepsy patients though provided more diffuse foci. Our findings can help in determining the surgical eligibility of a patient especially when MRI or video-EEG monitoring are non-localizing, and can help with placement of subdural grids and strips for EEG studies. © 2015 Elsevier B.V. All rights reserved.

PubMed | Oilfield General Hospital of Daqing and Harbin Medical University
Type: | Journal: Experimental biology and medicine (Maywood, N.J.) | Year: 2016

Gastric cancer is a common malignancy, and is one of the most frequent causes of cancer deaths worldwide. Recently, members of the transglutaminases (TGM) family, especially TGM2, have been implicated in the progression and drug resistance of cancers, but the function of TGM1 in cancer development has been largely overlooked. In this study, we demonstrate the roles of TGM1 in development of gastric cancer. We found that expression levels of TGM1 were upregulated in both gastric cancer tissues and cultured gastric cancer cells, and that TGM1 expression levels were correlated with patient survival. In cultured gastric cancer cells, loss of TGM1 expression inhibited cell proliferation and promoted apoptosis, as well increased gastric cancer cell sensitivity to chemotherapeutic drugs and reducing stemness. These results strongly supported the participation of TGM1 in the regulation of gastric cancer development. In addition, we found evidence that the mechanism of action of TGM1 in regulating gastric cancer cell might involve the Wnt signaling pathway, as loss of TGM1 expression in gastric cancer cells led to a significant suppression of Wnt signaling activities.

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