ABSTRACT
Objective:To investigate characteristics and differences of cerebral glucose metabolism in patients with anti- N-methyl- D-aspartate receptor (NMDAR) encephalitis from the perspective of different trigger factors of antibodies. Methods:A total of 15 patients (8 males, 7 females, age (30.5±17.7) years) with anti-NMDAR encephalitis between January 2016 and January 2019 in Huashan Hospital, Fudan University were recruited retrospectively. All patients underwent resting state cerebral 18F-FDG PET imaging. The characteristics of brain glucose metabolism were analyzed, and the SUV ratio (SUVR) was semi-quantitatively compared with that in 12 healthy subjects (HS; 7 males, 5 females, age (51.5±9.6) years). Independent-sample t test was used to analyze the data. Results:Among 15 patients, 5 patients were viral encephalitis-related anti-NMDAR encephalitis, showing focal decreased metabolism in unilateral temporal lobe or basal ganglia (SUVR: patients: 0.659±0.219; HS: 1.754±0.203; t=-9.58, P<0.001), with increased metabolism in contralateral temporal lobe or basal ganglia (SUVR: patients: 2.275±0.244; HS: 1.960±0.227; t=2.55, P=0.022) in 18F-FDG PET imaging. Six patients were cryptogenic anti-NMDAR encephalitis, showing asymmetric increased metabolism in frontal, temporal, parietal and basal ganglia (SUVR: patients: 2.482±0.395; HS: 1.754±0.203; t=5.23, P<0.001), with decreased metabolism in bilateral occipital lobes. The remaining 4 cases were paraneoplastic origin accompanied by teratoma, showing increased metabolism in bilateral temporal and basal ganglia (SUVR: patient: 2.359±0.181; HS: 1.960±0.227; t=3.16, P=0.007), with mild decreased metabolism in bilateral occipital lobe. Conclusions:The abnormal changes of cerebral glucose metabolism in patients with anti-NMDAR encephalitis can be divided into at least three patterns according to different trigger factors. A comprehensive understanding of these characteristic metabolic changes is helpful for detecting disease, and may provide potential value in indicating different causes.
ABSTRACT
Objective To investigate the effect of piR-9994 on the biological behavior of gastric cancer cells and its possible mechanism. Methods The expression of piR-9994 in gastric cancer cell lines (MGC803 and AGS) and normal gastric epithelial cells (GES-1) were detected by qRT-PCR. MGC803 cell line with piR-9994 overexpression and knockdown were constructed. The effects of piR-9994 expression changes on cell proliferation were detected by MTT and clone formation assay. The scratch wound healing assay and Transwell invasion assay were used to detect cell migration and invasion abilities. qRT-PCR and Western blot were used to detect cell proliferation and EMT-related genes expression. Results The expression level of piR-9994 in MGC803 cells was significantly higher than that in normal gastric epithelial cell line GES-1 (P < 0.05). The overexpression of piR-9994 promoted the proliferation, invasion and metastasis of gastric cancer cells, while piR-9994 knockdown had the opposite effect. piR-9994 expression was closely related to cell cycle, especially in S phase. The overexpression of piR-9994 promoted the expression of proliferation-related genes PCNA, CCND1 and Bcl-2, inhibited the expression of apoptosis gene C-PARP, and promoted the expression of EMT-related genes N-cadherin, MMP7, Twist and Vimentin; while piR-9994 knockdown had the opposite effect. Conclusion Abnormal expression of piR-9994 affects the proliferation, invasion, metastasis and EMT process of gastric cancer cells. piR-9994 may be a new biomarker and therapeutic target for gastric cancer.