0.05). It is included that these four concentrations of Se do not directly stimulate and inhibit the oxidizing activity of leucocyte.

0.05). The integral values of leucocyte chemiluminescence (cpm/leucocyte)were 7.267?0.855(Group A), 10.324 ?1.026(Group B) and13.061?1.589(Group C) repectively. Statistically there were a very significant difference(p0.05) between Group B and Group C. The results indicated thet Se had no effect on the tatal of leucocytes, a low level of Se decreased the leucophagocytic oxidative activity, but the Complement of Se can increase such activity. The resulte showed some evidence to the pattogenesis and clinical prevention and treatment of Keshan Disease.

Red cell immunologic adherent function and Se quantity were measured in 48 normal children of Keshan disease area and the reaction of red cell C3bR to these children. The results showed that the Se quantity and the rosette formation rate of red cell C3bR of normal children in Keshan disease area were significantly lower than that in the control(P0.05).

Objective:To investigate the clinical, neuropsychological, and neuroimage characteristics in patients with corticobasal syndrome (CBS), and to elucidate the exact diagnosis of CBS patients.Methods:Twelve CBS cases admitted to the Department of Neurology, Huashan Hosiptal,Fudan University from April 2019 to July 2021 were retrospectively enrolled in this study. Those data, including clinical features (demographic data and clinical characteristics of cortical dysfunction and movement disorder), neuropsychological assessment [Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) scales score], brain magnetic resonance imaging (MRI) and multi-mode positron emission tomography (PET)/CT, were collected and carefully reviewed. Exact diagnosis of these patients was given according to the disease diagnosis criteria.Results:Cortical dysfunction and asymmetrical movement disorders were found in all cases, with poor response to levodopa. Patients suffered from cognitive impairment (MMSE score 16.16±9.82, MoCA score 13.44±7.35). The cranial MRI demonstrated significant asymmetric atrophy of frontal and parietal lobes, especially in the pre- and post-central gyrus. Fluorodeoxyglucose PET of 12 patients showed asymmetric frontal lobe and basal ganglia (especially caudate and putamen) hypometabolism (obviously on the contralateral side of the affected limb). Tau PET was implemented in 11 patients and displayed that abnormal tau protein deposition was positive in the cortex and/or subcortex in all patients. Of the 4 cases, who completed amyloid PET, amyloid protein deposition was positive in the cortex of 2 patients. As a result, 6 patients were diagnosed as progressive supranuclear palsy, 1 patient was diagnosed as corticobasal degeneration, and 5 patients were diagnosed as Alzheimer′s disease.Conclusions:The etiology of CBS is heterogeneous. The combination of clinical manifestation, cranial MRI and multi-mode PET/CT helps the differential diagnosis of CBS.