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Is Chemokine Receptor CCR9 Required for Synovitis in Rheumatoid Arthritis? Deficiency of CCR9 in a Murine model of Antigen-Induced Arthritis

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Open Journal of Rheumatology and Autoimmune Diseases 2012年第4期2卷 77-84页

作者： Alison Cartwright Sophie King Jim Middleton Oksana Kehoe Faculty of Medicine and Dentistry School of Oral and Dental Sciences University of Bristol Bristol UK Keele University at Robert Jones and Agnes Hunt Orthopaedic Hospital Oswestry UK Keele University at Robert Jones and Agnes Hunt Orthopaedic Hospital Oswestry UK Faculty of Medicine and Dentistry School of Oral and Dental Sciences University of Bristol Bristol UK.

Objectives: Monocytes/macrophages accumulate in the synovial membrane in rheumatoid arthritis and play a key role in disease pathogenesis, contributing to inflammation, cartilage destruction and bone erosion. Identification of molecules involved in monocyte/macrophage recruitment in inflammation is crucial for development of therapeutic interventions. Chemokine receptor CCR9 is up-regulated on these cells in peripheral blood and synovium of rheumatoid patients. This study investigated the course of antigen-induced arthritis in CCR9 deficient C57BL/6 mice in comparison to wild type animals to determine whether CCR9 is critical for disease severity and progression. Methods: Methylated bovine serum albumin was used for induction of uni-lateral arthritis by direct injection into the knee joints of preimmunized animals. Arthritis is confined to the injected joint allowing comparison with the normal opposing joint. Clinical severity of arthritis was assessed by measuring swelling in the arthritic joint in comparison to the normal joint. Histological analysis was performed to assess the extent of leukocyte infiltration and cartilage depletion. Results: Levels of swelling were not significantly different between wild type and CCR9 deficient mice. Similarly there was no significant difference in histological severity of arthritis when comparing CCR9-deficient mice to wild type mice. Conclusions: CCR9 was not required for development of synovial inflammation and cartilage destruction in the anti-gen-induced model of arthritis in C57BL/6 mice in this study. This may reflect a true lack of a pathogenic role of CCR9 on monocyte/macrophage function in vivo or it may reflect differences in the current antigen-induced arthritis model when compared to human RA.

关键词： Chemokine Receptor CCR9 Rheumatoid Arthritis Inflammation Antigen-Induced Arthritis Mouse mod-el Monocytes/Macrophages

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Automatic Sleep Spindle Detection with EEG Based on Complex Demodulation Method and Decision Tree model

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Journal of Biomedical Science and Engineering 2017年第5期10卷 10-17页

作者： Jiabin Li Bei Wang Takenao Sugi Yu Zhang Masatoshi Nakamura Department of Automation East University of Science and Technology Shanghai China Department of electrical and electronic Engineering Saga University Saga Japan Research Institute of Systems Control Institute for Advanced Research and Education Saga University Saga Japan

Sleep spindle is the characteristic waveform of electroencephalogram (EEG) which is important for clinical diagnosis. In this study, an automatic sleep spindle detection method was developed. The EEG signals were recorded based on the standard polysomnogram (PSG) measurement. A preprocessing procedure is introduced to exclude the unnecessary data segments and normalized the necessary data segments. Complex demodulation method is adopted to detect the candidate sleep spindle waveforms and calculate the features. The sleep spindles are recognized based on a decision tree model. Finally, the detected sleep spindles were utilized to amend the sleep stage recognition results. The sleep EEG data from 3 patients with sleep disorders were analyzed. The obtained results showed that the detected sleep spindles in EEG signal improved the accuracy of sleep stage recognition.

关键词： Sleep Spindle Detection Complex Demodulation Method Decision Tree mod-el EEG

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