[Recognition of motor imagery electroencephalogram based on flicker noise spectroscopy and weighted filter bank common spatial pattern].

Due to the high complexity and subject variability of motor imagery electroencephalogram, its decoding is limited by the inadequate accuracy of traditional recognition models. To resolve this problem, a recognition model for motor imagery electroencephalogram based on flicker noise spectrum (FNS) and weighted filter bank common spatial pattern ( wFBCSP) was proposed. First, the FNS method was used to analyze the motor imagery electroencephalogram. Using the second derivative moment as structure function, the ensued precursor time series were generated by using a sliding window strategy, so that hidden dynamic information of transition phase could be captured. Then, based on the characteristic of signal frequency band, the feature of the transition phase precursor time series and reaction phase series were extracted by wFBCSP, generating features representing relevant transition and reaction phase. To make the selected features adapt to subject variability and realize better generalization, algorithm of minimum redundancy maximum relevance was further used to select features. Finally, support vector machine as the classifier was used for the classification. In the motor imagery electroencephalogram recognition, the method proposed in this study yielded an average accuracy of 86.34%, which is higher than the comparison methods. Thus, our proposed method provides a new idea for decoding motor imagery electroencephalogram.

Histiocytic Necrotizing Lymphadenitis Mimicking Acute Appendicitis in a Child: A Case Report.

Background: Histiocytic necrotizing lymphadenitis, also known as Kikuchi-Fujimoto disease (KFD), is a self-limiting inflammatory disease with low incidence and high misdiagnosis rate in children. Furthermore, cases where the clinical presentation resembles acute appendicitis are very rare. Case Presentation: A 14-year-old boy was misdiagnosed as acute appendicitis and received operative treatment at his early visit. He suffered from abdominal pain, vomiting, diarrhea, fever, and lymphadenitis at the ileocecal junction, which were found by B-ultrasonography examination and surgery. Lymphadenectomy, as well as appendectomy, was performed, and KFD was identified by pathological examination. The patient was transferred to our hospital for further therapy because of recurrent fever and abdominal pain after the appendectomy. His temperature became normal after methylprednisolone was administered, and no recurrence was observed till now during follow-up. Conclusions: Necrotizing lymphadenitis involving mesenteric lymph nodes may cause acute-appendicitis-like symptom; KFD should be a diagnostic consideration for mesenteric lymphadenitis.

mTOR Overactivation in Mesenchymal cells Aggravates CCl4- Induced liver Fibrosis.

Hepatic stellate cells are of mesenchymal cell type located in the space of Disse. Upon liver injury, HSCs transactivate into myofibroblasts with increase in expression of fibrillar collagen, especially collagen I and III, leading to liver fibrosis. Previous studies have shown mTOR signaling is activated during liver fibrosis. However, there is no direct evidence in vivo. The aim of this study is to examine the effects of conditional deletion of TSC1 in mesenchymal on pathogenesis of liver fibrosis. Crossing mice bearing the floxed TSC1 gene with mice harboring Col1α2-Cre-ER(T) successfully generated progeny with a conditional knockout of TSC1 (TSC1 CKO) in collagen I expressing mesenchymal cells. TSC1 CKO and WT mice were subjected to CCl4, oil or CCl4+ rapamycin treatment for 8 weeks. TSC1 CKO mice developed pronounced liver fibrosis relative to WT mice, as examined by ALT, hydroxyproline, histopathology, and profibrogenic gene. Absence of TSC1 in mesenchymal cells induced proliferation and prevented apoptosis in activated HSCs. However, there were no significant differences in oil-treated TSC1 CKO and WT mice. Rapamycin, restored these phenotypic changes by preventing myofibroblasts proliferation and enhancing their apoptosis. These findings revealed mTOR overactivation in mesenchymal cells aggravates CCl4- induced liver fibrosis and the rapamycin prevent its occurance.

[Differential gene expression profiling for identification of potential pathogenic genes and pathways in carotid unstable plaques].

OBJECTIVE: To explore the molecular mechanism in the formation of unstable plaques. METHODS: The cDNA microarray E-MTAB-2055 was downloaded from ArrayExpress database to screen the differentially expressed genes in 24 ruptured plaques against 24 stable plaques. Functional enrichment analysis was conducted to define the biological processes and pathways involved in disease progression. The protein-protein interaction network was constructed to identify the risk modules with close interactions. Five pairs of carotid specimens were used to validate 3 differentially expressed genes of the risk modules by real-time PCR. RESULTS: A total of 439 genes showed differential expression in our analysis, including 232 up-regulated and 207 down-regulated genes according to the data filter criteria. Immune-related biological processes and pathways were greatly enriched. The protein-protein interaction network and module analysis suggested that TYROBP, VCL and CXCR4 might play critical roles in the development of unstable plaques, and differential expressions of CXCR4 and TYROBP in carotid plaques were confirmed by real-time PCR. CONCLUSION: Our study shows the differential gene expression profile, potential biological processes and signaling pathways involved in the process of plaque rupture. TYROBP may be a new candidate disease gene in the pathogenesis of unstable plaques.